Necrosis

Presented
By
Ahmed El-Rashedy

Professor & Previous Head

of Pathology Department

Al-Azhar University

Necrosis

Prof. Dr. Ahmed Elrashedy

Def.:

An irreversible morphological changes in a living

tissue or cells on exposure to a lethal irritant.

N.B.:

Autolysis is complete cessation of energy production

and anabolic activities with continuation of the
catabolic and lytic activities of the released
lysosomal enzymes.
Differences between Necrosis and Autolysis
Necrosis

Autolysis

1. Duration

Ante-mortem.

Post-mortem.

2. Location

Localized area of a living body.

Whole body.

3. Inflammation Present (In the surrounding tissue).

Absent.

Prof. Dr. Ahmed Elrashedy

Pathogenesis:

Two essential processes:

1.Enzymatic digestion of the cell by one of these factors:
A. Lysosomes of the dead cells themselves.
B. Lysosomes of the surrounding immigrant inflammatory
leukocytes (Heterolysis).
2. Denaturation of the cell proteins.
Pathology (Morphological changes):

I)Cytoplasmic changes:
1) Increased eosinophilia (due to increased affinity of the
denatured proteins for eosin stain).
2) Vacuolated (due to enzymatic digestion of its organelles).
3) Calcification of the dead cells (dystrophic calcification;
deposition of calcium salts in the serum onto the dead cells).
4) Loss of striations: in the sarcoplasm of necrotic muscles.

Prof. Dr. Ahmed Elrashedy

II)Nuclear changes:
1. Early (reversible) :
Clumping of the chromatin into large aggregates
attached to the nuclear membrane & to the
nucleolus
2. Later (Irreversible):
1) Pyknosis: Small densely stained nucleus.
2) Karyorrhexis (Chromatorrhexis): Fragmented
nucleus.
3) Karyolysis
(Chromatolysis):
Progressive
dissolution and fading of the nucleus (due to the
hydrolytic action of lysosomal DNases).

Prof. Dr. Ahmed Elrashedy

Types of Necrosis:
1) Coagulative necrosis e.g. any organ infarction except
the brain.
2) Liquefactive necrosis e.g. brain infarction & abscess.
3) Caseous necrosis e.g. secondary tuberculosis.
4) Fat necrosis:
A. Traumatic fat necrosis: e.g. trauma to the female
breast.
B. Enzymatic fat necrosis: e.g. Acute hemorrhagic
pancreatitis.
5) Gangrenous necrosis:
A. Dry gangrene: e.g. in exposed areas as in limbs.
B. Moist or Wet gangrene: in internal organs as intestine.

Prof. Dr. Ahmed Elrashedy

I) Coagulative Necrosis
Incidence:
The most common type of necrosis.
Pathogenesis:
Sudden severe ischemia
Denaturation of
cellular proteins that blocks the proteolysis
of these dead cells
Removal of the
necrotic cells either by fragmentation &
phagocytosis of the cellular debris by
phagocytic leukocytes.
Pathology:
A. Gross: The necrotic tissue appears:
1.Firm.
2.Pale.
3.Triangular with base towards the capsule
of the organ.

Prof. Dr. Ahmed Elrashedy

B.L/M (City of Ghosts): This means:

1) Preserved general outline of the cells.
2) Loss of fine cellular details.
3) Loss or fragmentation of the cellular nuclei.
Examples:
1) Myocardial infarction.
2) Renal infarction.
3) Splenic infarction.
4) Pulmonary infarction.
5) Suprarenal infarction.
Complications:
1) Gangrene (due to invasion of the necrotic
tissue by saprophytic bacteria).
2) Loss of function of the necrotic area.
3) Dystrophic calcification of the necrotic area.

Myocardial infarction

Pulmonary infarction
(Darker pink area)

Prof. Dr. Ahmed Elrashedy

II) Liquefactive Necrosis

Pathogenesis:
Ischemia
proteolysis (by the action of powerful
hydrolytic enzymes) that is more prominent (rapid
liquefaction) than denaturation of cellular proteins
Pathology:
A. Gross: The necrotic tissue appears:
1.Soft.
2.Liquefied & forms a cyst filled with fluid &
debris.
B. L/M:
Like coagulative but with a cystic structure.
Site:
Fat-rich tissues as nervous tissue.
Examples:
1.Cerebral infarction.
2.Abscess in any organ particularly brain & breast.

Cerebral infarction

Prof. Dr. Ahmed Elrashedy

III) Caseous Necrosis

Pathogenesis:
Denaturation of the cellular proteins with slow
liquefaction i.e. it is a combination of coagulative &
liquefactive necrosis.
Pathology:
A. Gross: The necrotic tissue appears
1) Soft.
2) Friable.
3) Cheesy yellowish gray poultaciouslike debris,
hence, the name caseous necrosis.
B. L/M:
Homogenous structureless pink material surrounded by
a chronic inflammatory granulomatous reaction formed
of lymphocytes, plasma cells, histiocytes, giant cells
(Langhans) & fibroblasts.
Example:
Secondary T.B.

2ry Pulmonary T.B.

2ry T.B. Encephalitis

Prof. Dr. Ahmed Elrashedy

IV) Gangrenous Necrosis

Pathogenesis:
1. Sudden ischemia
Denaturation
of cellular proteins together with
liquefaction of the dead tissue by
the
bacteria
&
recruited
inflammatory
leucocytes
(heterolysis).
2. When denaturation is more
prominent, the process is termed
dry gangrene but when liquefaction
is more pronounced, the process is
termed wet or moist gangrene.

Dry gangrene in lower limb

Moist or Wet gangrene in

intestine

Prof. Dr. Ahmed Elrashedy

IV) Gangrenous Necrosis

Examples & Pathology:

1) Dry gangrene in lower limbs:

Occlusion of the artery with opening of
both venous & lymphatic drainage
adequate drainage of the offensive
gangrenous fluid through these opened
vessels dry shriveled gangrenous part.

2)

Dry gangrene in lower limb

Moist or Wet gangrene in internal

organs as intestine:
There is obstruction of both venous
drainage & accompanied artery ,thus, no
drainage of the offensive gangrenous
fluid that accumulates in the affected part
causing its swelling & enlargement.

Moist or Wet gangrene in

intestine

Prof. Dr. Ahmed Elrashedy

V) Fat Necrosis
Pathogenesis:
Increased lipolysis in fat rich organs
occurring by trauma or release & activation of
lipase by damage of the pancreatic duct.
Examples:
1.Traumatic fat necrosis:
e.g. Trauma to a female breast.
Pathology:
Trauma activates lipolysis that liquefies fatty
tissue which is surrounded by a granulomatous
reaction formed of lipid-laden or foamy
macrophages (phagocytic cells eating liquefied
lipid) together with lymphocytes, plasma cells,
foreign body giant cells & fibroblasts.

Traumatic fat necrosis in

breast

Prof. Dr. Ahmed Elrashedy

V) Fat Necrosis
2) Enzymatic fat necrosis:

e.g. Acute
hemorrhagic
pancreatitis
(Acute
pancreatic necrosis):
This is accompanied with a release &
activation of pancreatic lipase destruction
& lysis of the pancreatic tissue as well as
the fat depots throughout the abdomen
(Omentum & fat about the pancreas)
causing
Disintegration of the neutral
fat into free fatty acids which combines
with
intestinal
calcium
forming
calcium soaps (Chalky white deposits on
the intestine).

Prof. Dr. Ahmed Elrashedy

2) Enzymatic fat necrosis

Pathology:
Gross: The affected intestine is:
1. Firm.
2. Shows chalky white foci.
L/M:
1) Shadow of lipolyzed necrotic tissue
surrounded by an inflammatory reaction
formed of lipid-laden macrophages,
lymphocytes , plasma cells & giant cells.
2) Amorphous bluish calcified areas
(stained black by Van Kossa stain).



Prof. Dr. Ahmed Elrashedy