Coagulative necrosis and its organ manifestation

1. Definition & Mechanism

• Coagulative necrosis (凝固壊死): cells are dead but the basic tissue architecture (cell outlines) is preserved; texture becomes firm.
• Injury denatures proteins and enzymes → proteolysis is blocked → “ghost” cells.
• Denatured proteins bind eosin → eosinophilia of anucleate cells.
• Inflammatory cells later migrate in and digest the dead tissue.
• Primarily in the heart, kidney, spleen (classically ischemia — brain is the exception).

2. Infarct — Classified by Colour

• White (anemic) infarct — inflow problem; arterial occlusion in solid organs (heart, spleen, kidney) where density limits haemorrhage.
• Red (hemorrhagic) infarct — drainage problem; venous occlusion, loose tissues, dual circulation (lung, intestine), or after reperfusion.

Anemic (inflow)	Hemorrhagic (drainage / reperfusion)
Renal infarct	AMI after reperfusion
Splenic infarct	Pulmonary infarct
Dry gangrene	Intestinal infarct

3. Organ Manifestations

Renal infarct

• Causes: thrombosis (atherosclerotic plaque) or embolism (90% from heart — AF in left atrium, LV aneurysm, aortic stenosis).
• Morphology: pale, wedge-shaped necrosis, apex toward medulla, hyperemic rim; heals with fibrous scar.
• Clinical: usually silent; possible hypertension (RAAS activation).

Splenic infarct

• Similar to renal; almost always embolic. Pale wedge-shaped, capsule often fibrin-covered; heals with depressed scar; usually silent.

Dry gangrene (gangrena sicca)

• Reduced flow to lower limbs (femoral/popliteal occlusion) → distal-to-proximal mummified, black tissue (Hb + H₂S → iron sulfide); claudicatio intermittens.

Acute myocardial infarction (AMI)

• Usually hemorrhagic because tissue is reperfused and vessels are leaky (see A/08).

Pulmonary infarct (dual circulation)

• Cause: embolism from deep vein thrombosis (femoral/iliac/popliteal).
  • Large/saddle embolus → sudden death, no time for morphologic change.
  • Medium/small → endothelial damage → haemorrhage.
• Infarct only if CHF/impaired bronchial circulation: lower lobes, wedge-shaped (apex to hilum), red-blue → red-brown (hemosiderin) → white scar.
• ~60–80% clinically silent; large emboli → ↑pulmonary pressure, ↓cardiac output, right heart failure, hypoxemia.

Intestinal infarct (dual SMA/IMA)

• SMA thrombus → necrosis of duodenum/jejunum → haemorrhage, peritonitis, septic shock.
• IMA thrombus → usually compensated by SMA.
• Portal vein thrombus → haemorrhagic necrosis of whole intestine.
• Subtypes: mucosal (often reversible) → mural → transmural (gangrene, perforation; ~90% mortality).

💡 High-yield: Wedge-shaped pale infarct with preserved “ghost” outlines in heart/kidney/spleen = coagulative necrosis. Cardiac emboli (AF, LV aneurysm) are the classic source of renal/splenic infarcts.