STEPTRACKERGENERAL PRINCIPLES | PATHOLOGY | HIGH-YIELD REVIEW

Necrosis Patterns

Death of groups of cells, always followed by inflammation — the pattern depends on the organ and the trigger.

FOCUS ON
Match pattern to organ and cause. Most solid-organ infarcts are coagulative, but the brain is liquefactive. Caseous means granuloma (TB, fungi). Chalky white deposits in peripancreatic fat mean fat necrosis with saponification.
PATTERN
MECHANISM · APPEARANCE
WHERE · CAUSE
CLASSIC CLUE
Coagulative
protein denaturation wins
Enzymes denatured with the structural proteins, so cell outlines are preserved ("ghost cells"); cytoplasm eosinophilic, nuclei lost.
Ischemic infarct of any solid organ except brain — heart, kidney, spleen, liver.
Wedge-shaped, pale infarct with its base at the organ surface
Liquefactive
enzymatic digestion wins
Neutrophil lysosomal enzymes or brain microglia digest tissue into fluid; leaves a cyst or cavity.
Brain infarct · bacterial abscess · pancreatic parenchyma in acute pancreatitis
Cystic cavity weeks after a stroke; pus-filled abscess
Caseous
"cheese-like"
Mix of coagulative and liquefactive; amorphous granular debris surrounded by a granuloma.
Tuberculosis, systemic fungi (Histoplasma, Coccidioides), Nocardia
Soft white center inside a granuloma with giant cells
Fat necrosis
saponification
Released fatty acids bind Ca²⁺ → chalky white deposits, basophilic on H&E (dystrophic calcification).
Enzymatic: lipase in acute pancreatitis (peripancreatic fat). Traumatic: breast after injury.
Breast mass after seatbelt injury may mimic carcinoma
Fibrinoid
vessel wall
Immune-complex or pressure damage lets plasma proteins leak into the wall → bright pink, fibrin-like smudge.
Vasculitis, malignant hypertension, placental vessels in preeclampsia
Bright pink arteriole walls on H&E
Gangrenous
limb or bowel
Dry: coagulative necrosis from ischemia. Wet: superimposed infection adds liquefaction.
Lower limb (diabetes, peripheral artery disease), GI tract (volvulus, strangulated hernia)
Black shriveled toe (dry) vs swollen, foul limb (wet)

Mechanism — which force wins?

Lethal injuryMembranes fail
→
Denaturation > digestionCoagulative
→
Digestion > denaturationLiquefactive
→
InflammationNeutrophils, then macrophages
→
OutcomeScar (most organs) or cyst (brain)

Necrosis spills cell contents, so it always provokes inflammation. Apoptosis does not (page 1.04).

Red vs pale infarcts

TYPE
WHY
ORGANS
Pale (white)
Dense solid organ with end-arteries; blood cannot re-enter
Heart, kidney, spleen
Red (hemorrhagic)
Loose tissue, dual or collateral supply, or reperfusion
Lung, liver, small intestine, testis/ovary torsion
Reperfused
Blood returns into dead tissue (e.g., after thrombolysis)
Heart after reperfusion becomes red
Septic
Infected embolus (endocarditis) seeds the infarct
Brain, spleen, kidney — abscess forms

How it's tested

COMMON CONFUSIONThe brain is the exception: ischemia there gives liquefactive necrosis, not coagulative. Pancreatitis gives both — liquefactive in the gland, fat necrosis around it.
THE TRAP"Chalky white foci in mesenteric fat" in an alcoholic with epigastric pain is saponification. That is dystrophic calcification, so serum calcium is normal or even low.
YOUR APPROACHOrgan first (brain → liquefactive), then trigger: abscess → liquefactive; granuloma → caseous; lipase or trauma → fat; vessel wall → fibrinoid; limb → gangrene.

If you see… think…

Wedge-shaped pale kidney infarct with ghost cells → coagulative necrosis
Cystic cavity weeks after a stroke → liquefactive necrosis
Upper-lobe lesion with cheesy center inside a granuloma → caseous (TB)
Acute pancreatitis + chalky white spots + low Ca²⁺ → enzymatic fat necrosis
Breast lump after trauma, calcified on mammogram → traumatic fat necrosis
Bright pink arterioles in malignant hypertension → fibrinoid necrosis
Diabetic, black dry toe → dry gangrene; swollen and foul → wet gangrene
Hemorrhagic testis after torsion → red infarct
Pus-filled cavity of neutrophils → abscess (liquefactive)