Colliquative necrosis and its organ manifestation

1. Definition & Mechanism

• Colliquative / liquefactive necrosis (融解壊死・液化壊死): enzymes are active and digest the tissue into a liquid, viscous mass; cell outlines are not preserved.
• Enzyme source: heterolysis (inflammatory-cell enzymes) or autolysis (cell’s own enzymes).
• Typical of bacterial/fungal infections (microbes recruit inflammatory cells) and CNS infarction.
• Creamy yellow appearance from dead leukocytes (pus) → abscess.

Anemic (inflow)	Hemorrhagic (drainage)
Cerebral infarct	Cerebral infarct (haemorrhagic)
Wet gangrene; pulmonary abscess

2. Cerebral Infarct (brain = exception to coagulative rule)

• Causes: thrombus (atherosclerosis at carotid bifurcation, MCA, basilar tip) or embolus (often cardiac mural thrombus, more common).
• Morphology: perifocal edema, BBB damage, tissue “disappears”; demarcation by edema (not neutrophils).
• Encephalomalacia (brain softening) stages:
  1. Alba — first 36–48 h, swollen/soft; macrophages by day 3 → pale.
  2. Flava — liquefactive digestion → yellow.
  3. Cysta post-encephalomalacia — fluid-filled cyst; gliosis (astrocyte proliferation/hypertrophy) at the margin.
  4. Rubra (hemorrhagic) — red, from reperfusion, venous thrombus, or border-zone (watershed) necrosis (e.g. circle of Willis).

3. Wet Gangrene (gangrena humida)

• Coagulative necrosis + superimposed infection → progresses to liquefactive.
• Moist tissues (mouth, bowel, lung, cervix, vulva); edematous, soft, dark.
• Bacterial toxins absorbed → free communication with circulation → sepsis.

4. Pulmonary Abscess

• Localized necrosis → pus-filled cavity rimmed by inflammatory cells (bacterial toxins lyse tissue).
• Causes: aspiration (teeth/sinuses/tonsils/GI → usually right lung), pneumonia/bronchial obstruction (multiple, basal), septic emboli/hematogenous (multiple, anywhere).
• Clinical: cough with bloody/purulent sputum, fever, anaemia, weight loss.
• Complications: rupture → bronchopleural fistula, pneumothorax, empyema.

💡 High-yield: The brain undergoes liquefactive (not coagulative) necrosis after infarction, leaving a fluid-filled cyst with surrounding gliosis. Pus = liquefactive necrosis driven by neutrophil enzymes.