Learning Objective
By the end of this lesson, the learner will be able to identify different types of necrosis, describe their mechanisms, recognize clinical causes, and correlate them with characteristic microscopic and gross features.
Necrosis
Necrosis is a pathologic cell death due to external injury, causing:
- Plasma membrane disruption
- Leakage of intracellular contents
- Enzymatic digestion and denaturation
- Local inflammatory reaction (unlike apoptosis)
Necrosis triggers neutrophils and macrophages due to released intracellular molecules acting as DAMPs (damage-associated molecular patterns).
Types of Necrosis
1. Coagulative Necrosis
Seen In
- Most ischemic/infarcted tissues
- Exception: brain
Mechanism
- Injury → protein denaturation → enzymes are also denatured → proteolysis is inhibited
Histologic Appearance
- Preserved cell outlines & architecture
- Loss of nuclei
- Increased eosinophilia (bright pink cytoplasm)
Typical Example
- Myocardial infarction
- Renal infarction
2. Liquefactive Necrosis
Seen In
- Bacterial infections (abscesses)
- CNS infarcts
Mechanism
- Neutrophils release lysosomal enzymes → digestion and liquefaction of tissue
Histology
- Early: necrotic debris + neutrophils
- Later: cystic spaces, cavitation, microglial phagocytosis in CNS
Examples
- Brain infarction
- Lung abscess
- Liver abscess
3. Caseous Necrosis
Seen In
- Tuberculosis
- Systemic fungal infections
(e.g., Histoplasma capsulatum) - Nocardia infections
Mechanism
- Macrophages wall off organisms → granuloma formation
Histology
- Fragmented, granular cells
- Surrounded by macrophages, epithelioid histiocytes, and lymphocytes
- “Cheesy” gross appearance
Gross Finding
- Soft, crumbly, white-yellow necrosis
4. Fat Necrosis
Two forms:
A. Enzymatic Fat Necrosis
Seen in:
- Acute pancreatitis
→ pancreatic lipase escapes into the peripancreatic fat
Mechanism
- Triglycerides → free fatty acids
Free fatty acids + Ca²⁺ → saponification (soap formation)
Histology
- Chalky-white deposits
- Blue saponification deposits on H&E
B. Traumatic Fat Necrosis
Seen with:
- Breast trauma
Produces:
- Rupture of fat cells
- Inflammatory reaction
5. Fibrinoid Necrosis
Seen In
- Immune-mediated vasculitis
e.g., Polyarteritis nodosa - Severe hypertension
- Preeclampsia
- Malignant hypertension
Mechanism
- Immune complexes + fibrin leak → vessel wall degeneration
Histology
- Eosinophilic, protein-rich material in the vessel wall (“fibrin-like”)
6. Gangrenous Necrosis
Occurs in the distal extremities or bowel after chronic ischemia.
Two Subtypes
A. Dry Gangrene
- Due to ischemia alone
- Coagulative necrosis pattern
- Dry, shrunken, black tissue
B. Wet Gangrene
- When an infection superimposes
- Liquefactive necrosis over coagulative
- Swollen, foul-smelling, fluid-filled tissue
Activity
Summary Table of Necrosis Types
| Type | Typical Cause | Key Feature | Appearance |
|---|---|---|---|
| Coagulative | Ischemia (except brain) | Proteins denature → architecture preserved | Red/pink eosinophilic cells without nuclei |
| Liquefactive | Bacterial abscess, CNS infarct | Enzyme digestion of tissue | Cystic cavity, pus |
| Caseous | TB, fungi | Granuloma formation | Soft “cheesy” debris |
| Fat | Pancreatitis, trauma | Saponification | Chalky deposits |
| Fibrinoid | Vasculitides, HTN disorders | Immune complex deposition | Pink fibrin-like material in vessel walls |
| Gangrenous | Chronic ischemia (limbs, GI) | Dry = coagulative; Wet = infectious liquefactive | Black, necrotic tissue |










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