General pathology · Cell injury, adaptation and death
Patterns of necrosis: coagulative, liquefactive, caseous, fat, fibrinoid, gangrenous !
- Lesion
Dead tissue looks different depending on the organ and the cause. The pattern on the slide is a clue to what happened.
Updated 2026-11-01
What it is
Necrosis is the death of groups of cells in living tissue, with membrane rupture and inflammation. Whether proteins coagulate or enzymes digest the tissue decides the look. Six classic patterns are recognised; they are morphological descriptions, and each one points to typical organs and causes.
Structure
- Early necrosis (hours): increased eosinophilia from lost RNA and denatured proteins; nuclei still visible.
- Nuclear changes appear next: pyknosis, karyorrhexis, then karyolysis.
- Neutrophils arrive at the edge in one to three days; macrophages clear debris later.
- Old necrotic foci may calcify (dystrophic calcification), as in old tuberculous granulomas.
The six patterns at a glance
| Pattern | Why it looks that way | Gross and microscopic | Typical setting |
|---|---|---|---|
| Coagulative | Acidosis denatures structural proteins and enzymes, so the cells are not digested for days | Firm, pale tissue; eosinophilic cells without nuclei, outlines preserved | Myocardial, renal and splenic infarcts |
| Liquefactive | Enzymes from neutrophils or the tissue itself digest the dead cells | Soft or liquid cavity; pus in abscesses | Brain infarct, bacterial or fungal abscess |
| Caseous | Granulomatous reaction to an agent such as Mycobacterium tuberculosis | White, crumbly, cheese-like; amorphous granular debris ringed by a granuloma | Tuberculosis, histoplasmosis |
| Fat | Released lipases split fat; fatty acids bind calcium (saponification) | Chalky white spots; pale fat-cell outlines with basophilic calcium | Acute pancreatitis; breast trauma |
| Fibrinoid | Immune complexes and plasma proteins leak into the vessel wall | Bright pink, smudgy, fibrin-like wall; not visible grossly | Polyarteritis nodosa, malignant hypertension |
| Gangrenous | Ischemic coagulative necrosis of a limb; liquefaction if infection is added | Dry: black, shrunken; wet: swollen, foul and spreading | Diabetic foot, peripheral artery disease |
Clinical notes
- Gas gangrene from Clostridium perfringens causes crepitus and rapid spread and is a surgical emergency.
- Tuberculosis remains common in Colombia; caseating granulomas on a biopsy prompt cultures and molecular tests for mycobacteria.
Test yourself
Think of the answer, then tap the question to see it.
Why does ischemia of the brain cause liquefactive rather than coagulative necrosis?
Brain tissue has little structural protein and abundant lipids and lytic enzymes, so the dead tissue is digested into a liquid mass.
What makes the chalky white spots of fat necrosis in acute pancreatitis?
Lipases release fatty acids that combine with calcium to form soaps (saponification).
In which conditions is fibrinoid necrosis seen?
Immune complex vasculitis (such as polyarteritis nodosa) and malignant hypertension.
What is the difference between dry and wet gangrene?
Dry gangrene is coagulative necrosis of an ischemic limb; wet gangrene adds bacterial infection and liquefactive necrosis.
Related
- Apoptosis vs necrosis: the comparison table
- Reversible vs irreversible cell injury: the point of no return
- Pathologic calcification: dystrophic vs metastatic
- Granulomatous inflammation: caseating vs non-caseating, the causes to know
- Infarction: red vs white, and what decides the damage
- The myocardial infarct over time: what the pathologist sees from hours to months
Related conditions
- Myocardial Infarction (Heart Attack)
- Ischaemic stroke
- Tuberculosis
- Pulmonary tuberculosis
- Acute pancreatitis
- Necrotizing soft tissue infection (necrotizing fasciitis, gas gangrene)
- Diabetic foot
- Brain abscess
- Polyarteritis nodosa
- Hypertensive emergency and urgency
- Peripheral artery disease
- Frostbite
- Histoplasmosis
- Avascular necrosis of the femoral head
- Renal papillary necrosis
Elsewhere in DurgiPedia
- Cell injury, apoptosis and necrosis
- Granulomatous inflammation
- Microscopy and stains: H&E, PAS, trichrome, silver, immunohistochemistry
- Type III hypersensitivity (immune complexes)
Microorganisms
Educational content on the mechanisms of disease; not a diagnostic or treatment guide and no substitute for a health professional's advice. No doses are given.
Sources: Acute Pancreatitis (StatPearls (NCBI Bookshelf), 2024); Gangrene: MedlinePlus Medical Encyclopedia (MedlinePlus, US National Library of Medicine, 2024); Tuberculosis | TB | MedlinePlus (MedlinePlus, US National Library of Medicine, 2024).
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Representative model, for educational purposes only.