A BRIEF about GANGRENE

CHANGES AFTER CELL DEATH
Two types of pathologic changes may superimpose following
cell injury: gangrene (after necrosis) and pathologic calcifi -
cation (after degenerations as well as necrosis).

GANGRENE
Gangrene is necrosis of tissue associated with superadded
putrefaction, most often following coagulative necrosis due to
ischaemia (e.g. in gangrene of the bowel, gangrene of limb).
On the other hand, gangrenous or necrotising infl ammation is
characterised primarily by inflammation provoked by virulent
bacteria resulting in massive tissue necrosis. Thus, the endresult
of necrotising infl ammation and gangrene is the same
but the way the two are produced, is diff erent. The examples
of necrotising infl ammation are: gangre nous appendicitis,
gangrenous stomatitis (noma, cancrum oris).
There are 2 main types of gangrene—dry and wet, and
a variant of wet gangrene called gas gangrene. In all types of
gangrene, necrosis undergoes liquefaction by the action of
putrefactive bacteria.

Dry Gangrene
Th is form of gangrene begins in the distal part of a limb due
to ischaemia. Th e typical example is the dry gangrene in the toes and feet of an old patient due to severe atherossclerosis.

Other causes of dry gangrene foot include thromboangiitis

obliterans (Buerger’s disease), Raynaud’s disease, trauma,

ergot poisoning. It is usually initiated in one of the toes which

is farthest from the blood supply, containing so little blood that

even the invading bacteria fi nd it hard to grow in the necrosed

tissue. Th e gangrene spreads slowly upwards until it reaches

a point where the blood supply is adequate to keep the tissue

viable. A line of separation is formed at this point between the

gangrenous part and the viable part.

MORPHOLOGIC FEATURES Grossly, the aff ec ted part

is dry, shrunken and dark black, resemb ling the foot of

a mummy. It is black due to liberation of haemoglobin

from haemolysed red blood cells which is acted upon by

hydrogen disulfi de (H2S) produced by bacteria resulting in

formation of black iron sulfi de. Th e line of separation usually

brings about complete separation with eventual falling off

of the gangrenous tissue if it is not removed surgi cally (i.e.

spontaneous amputation) (Fig. 2.29).

Histologically, there is necrosis with smudging of the tissue.

Th e line of separation consists of infl am matory granulation

tissue (Fig. 2.30).

Wet Gangrene

Wet gangrene occurs in naturally moist tissues and organs such

as the bowel, lung, mouth, cervix, vulva etc. To other examples

of wet gangrene having clinical signifi cance are as follows:

 Diabetic foot which is due to high glucose content in the

necrosed tissue which favours growth of bacteria.

 Bed sores occurring in a bed-ridden patient due to pressure

on sites like the sacrum, buttocks and heel.

Wet gangrene usually develops due to blockage of both

venous as well as arterial blood fl ow and is more rapid.

Th e aff ected part is stuff ed with blood which favours the

rapid growth of putrefactive bacteria. Th e toxic products

formed by bacteria are absorbed causing profound systemic

manifestations of septicaemia, and fi nally death. Th e spreading

wet gangrene generally lacks clear-cut line of demarcation and

may spread to peritoneal cavity causing peritonitis.

MORPHOLOGIC FEATURES Grossly, the aff ected part is

soft, swollen, putrid, rotten and dark. Th e classic example

is gangrene of the bowel, commonly due to strangulated

hernia, volvulus or intussuscep tion. Th e part is stained

dark black due to the same mecha nism as in dry gangrene

Histologically, there is coagulative necrosis with stuffi ng

of aff ected part with blood. Th e mucosa is ulcerated

and sloughed. Lumen of the bowel contains mucus and

blood. Th ere is intense acute infl ammatory exudates and

thrombosed vessels. Th e line of demarcation between

gangrenous segment and viable bowel is generally not clearcut

GAS GANGRENE 

It is a special form of wet gangrene caused

by gas-forming clostridia (gram-positive anaerobic bacteria)

which gain entry into the tissues through open contaminated

wounds, especially in the muscles, or as a complication

of operation on colon which normally contains clostridia.

Clostridia produce various toxins which produce necrosis and

oedema locally and are also absorbed producing profound

systemic manifes tations.

MORPHOLOGIC FEATURES Grossly, the aff ected

area is swollen, oedematous, painful and crepitant due to

accumulation of gas bubbles of carbon dioxide within the

tissues formed by fermentation of sugars by bacterial toxins

Subsequently, the aff ected tissue becomes dark black and is

foul smelling.

Microscopically, the muscle fi bres undergo coagu lative

necrosis with liquefaction. Large number of gram-positive

bacilli can be identifi ed. At the peri phery, a zone of

leucocytic infi ltration, oedema and conges tion are found.

Capillary and venous thrombi are common.