M.
Shuja Tahir
Faisalabad, Pakistan
Surgery
GANGRENE
G angrene is the death (massive
necrosis) of macroscopic part of
the tissue with super-imposed
putrefaction.
ETIOLOGY
It is caused by the tissue ischaemia
secondary to following conditions :
ARTERIAL OBSTRUCTION
Acute or chronic obstruction to the flow
of arterial blood leads to gangrene
formation.
The arterial obstruction occurs due to ;
! Atherosclerosis.
! Thrombosis.
! Embolus (from atrial fibrillation).
! Post diabetic neuropathic arteritis.
! Constriction ring of strangulated
loops of bowel in volvulus and
strangulated hernias.
! Buerger's disease (thrombo-angitis
obliterans).
! Raynaud's disease.
! Cervical rib.
! Ergot poisoning.
! Tourniquets, tight plaster and
bandages.
! Intra arterial injection of
thiopentone or sclerosing
substances.
INFECTION
The anaerobic infections may lead to
various types of gangrene.
Following organisms commonly cause
2
the infections leading to gangrene ;
! Clostridial infection.
! Non clostridial anaerobic
infection.
! Staphylococcal infection.
164 April to June, 2010
IR-024
!
!
!
Streptococcal infection.
Bacteroides infection.
Mixed infection.
TRAUMA
The injured tissue leads to loss of blood
supply and death of major part of distal
tissue in following conditions ;
! Crush injuries.
! Pressure sores.
! Circumferential burns.
VENOUS OBSTRUCTION
The common diseases causing venous
obstruction and gangrene are ;
! Polycythemia.
! Pancreatic neoplasms.
! Trousseau's syndrome.
These may lead to peripheral venous
thrombosis which leads to retrograde
arterial obstruction and gangrene
formation.
TYPES OF GANGRENE
Following clinical varieties of the
gangrene are seen ;
! Dry gangrene.
! Moist or wet gangrene.
! Gas gangrene.
! Infective gangrene.
! Carbuncle.
! Meleney's synergistic gangrene.
! Fournier's gangrene.
! Cancrum oris and noma
vulvae.
DRY GANGRENE
This is not true gangrene and should be
called mummification. There is massive
necrosis but putrefaction is almost
negligible. Although putrefactive
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organisms are present but their growth
and activity is very much limited.
The typical odor of gangrene is
minimal. This is due to slow and
progressive occlusion of the arteries
supplying the gangrenous area.
The gangrenous part is black, dry and
of the original shape. It is just mummi-
fied. The line of demarcation is very
clear and separates the gangrenous
area from healthy area eventually
leading to auto-amputation.
WET (MOIST) GANGRENE
There is massive tissue necrosis and
plenty of moisture. The putrefactive
organisms grow rapidly and are very
active.
The gangrene spreads rapidly. The
gangrenous area is black, swollen and
smelly. The line of demarcation is not
clear as the gangrene spreads rapidly.
There is large area of cellulitis at the
junction of gangrenous area and
healthy area.
Toxaemia is very common in this type of
gangrene. Septic shock syndrome and
death of the patient may occur if not
treated adequately and in time.
This is usually secondary to sudden
occlusion of the arterial supply and
venous drainage. It also follows
infection and is associated with
diseases such as diabetes mellitus.
GAS GANGRENE
It is a life threatening condition. This
occurs due to infection with gas-
forming organisms. The infection with
gas forming clostridia causes.
Myositis in the presence of dead or
April to June, 2010 INDEPENDENT
damaged muscles and foreign bodies.
The local infection is associated with
liquefaction and gas formation.
The common causative organisms are ;
! Clostridium perfringens (cl.
welchii).
! Clostridium Novyi (cl. oedema-
tiens).
! Clostridium septicum.
Progressive putrefaction is caused by
Cl. Sporogenies and Cl. histolyticum.
The clostridia causing it produce potent
toxins such as ;
! Hyaluronidase.
! Collagenase.
! Haemolysins.
! Lecithinase.
! Other toxins.
It is a rare problem (0.1/100,000
3
/annum) .
It can follow an exogenous infection
from accidents, gun shot and other
injuries leading to severe tissue
damage with contamination, or
endogenous infection from one's own
intestinal tract.
There is gross necrosis, putrefaction
and gas formation.
This is common after severe trauma,
roadside accidents, high velocity
missile injuries, perineal injuries and
above knee amputations.
It is characterized by profound toxemia,
extensive local edema, massive
necrosis and variable degree of gas
formation.
There is no fibrosis or leukocytic
REVIEWS 165
 reaction.
The exotoxins produce cellulitis and
progressive myonecrosis. These also
ferment muscle carbohydrates and
produce lactic acid and gas (H2CO2)
leading to fishy odor and greenish
black appearance.
There is marked edema and enzymatic
necrosis of muscles commonly 24-72
hours after trauma.
Extensive exudate lacking in
inflammatory cells is present. The
affected region is swollen and large
bullous vesicles are present on the skin
which rupture.
Inflammed muscles show massive
myonecrosis. The muscles are soft,
black, friable and semifluid due to
action of proteolytic enzymes.
Gas bubbles are also present due to
bacterial fermentation of the necrotic
tissue.
Microscopically there is myonecrosis,
extensive haemolysis and marked
vascular injury with thrombosis.
There is widespread formation of gas
bubbles. The neuropathologic
1
changes are usually non specific .
The mortality rate in treated patients
varies between 25-40%. Untreated
2
patients have almost always fatal end .
Septic shock syndrome is also
accompanied by haemolytic anaemia,
renal failure and jaundice.
End stage of gas gangrene may show
foamy liver and presence of gas
bubbles in other viscera as well.
166 April to June, 2010
Gas gangrene is diagnosed clinically.
Dirty and infected wound is present with
lot of necrotic tissue and features of
septicaemia.
On palpation there is crepitus at local
area.
Plain x-ray of the area shows presence
of gas in subcutaneous tissue in
patients with gas gangrene
SYNERGISTIC GANGRENE
It is progressive gangrenous infection
of the skin, fascia and areolar tissue2.
It is progressive bacterial gangrene. It
commonly involves skin and
subcutaneous tissue. It is caused by the
synergistic action of micro-aerophilic
non-haemolytic streptococci and
anerobes.
It occurs a week or two weeks after the
infection. It spreads very quickly unless
treated adequately.
Burrowing ulcers (Meleny's ulcers) are
seen with gangrenous skin on the
edges. There is gross necrosis of large
areas of skin. The necrosis of sub
cutaneous tissue extends far beyond
the gangrenous skin.
Non clostridial gas gangrenous
cellulitis is usually caused by B.
melaninogenicus and anaerobic
streptococci.
CANCRUM ORIS AND NOMA VULVAE
These are types of infective gangrene of
muco-cutaneous junctions of mouth
and vulva.
These are seen in mal-nourished
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children with infective lesions such as
measles or chest infection
There is slow necrosis of the tissue and
death may occur due to inhalation
pneumonia.
FOURNIER'S GANGRENE
It is a condition similar to synergistic
gangrene. It is necrotizing fasciitis
spreading rapidly along facial planes,
muscles, subcutaneous tissue and skin.
There is subcutaneous edema. There is
dermal gangrene and appearance of
sero-sanguinous discharge.
It occurs probably due to thrombosis of
perforating vessels. The area involved
is usually scrotum, penis or both.
Systemic toxicity may lead to septic
shock syndrome3.
It is often associated with high
morbidity and mortality.
Surgical debridement, broad spectrum
antibiotics and use of hyperbaric
oxygen followed by plastic recons-
tructive procedures are used to
4,5
improve the survival of patients .
URAEMIC GANGRENE SYNDROME
It is the cutaneous gangrene seen in
patients with chronic renal failure and
hyperparathyroidism. It is associated
with vascular calcinosis and local
ischaemia6.
PYODERMA GANGRENOSUM
It is the infected cutaneous gangrene.
It is a rare, recurrent and chronic
condition.
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It presents as progressive papulo-
pustular lesion or large necrotic sterile
ulcers.
It follows systemic disorders such as
inflammatory bowel disease, rheu-
matoid arthritis, para-proteinemias,
haemotologic malignancies and other
malignant solid tumors.
There is rapid improvement after
treatment of the cause7.
TREATMENT OF IMPENDING
GANGRENE
The causes leading to gangrene are
treated and blood supply of the area is
improved as soon as possible.
Treatment of general diseases such as
diabetes mellitus, hypertension, atrial
fibrillation and peripheral ischaemia is
performed.
Smoking should be stopped
immediately.
The area at risk should be carefully
protected form minor trauma as well.
Slight pressure by ill fitting shoes can be
detrimental and may lead to gangrene
formation.
Vasodilator drugs may be used for the
improvement of local blood supply.
Sympathectomy whether surgical or
chemical is helpful in the treatment of
peripheral ischaemia.
Anticoagulants can be used in
gangrene secondary to thrombo-
embolic causes.
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 TREATMENT OF ESTABLISHED In cases of dry gangrene, one should
GANGRENE try to keep it dry and nothing more
Analgesics are required to relieve the should be done and one should wait
pain. for auto-amputation.

Intra-venous fluids and blood In cases of gas gangrene following

transfusion is given if so required. management is performed ;

Appropriate antibiotics are given ! Wound debridement.

intravenously.
The gangrenous area is excised
(amputation or resection) and repair
and restoration of the remaining tissue
is performed (anastomosis in case of
intestine and stump formation in case
of limbs).
! Excision of necrotic tissue.
! Wound toilet and appropriate
antibiotics.
! Anti-gas gangrene vaccination is
given parenterally.
! Hyperbaric oxygen may be of help
in limiting the growth of causative
anaerobic organisms.

REFERENCES
1. John Saunders Franz Von. Lichtenberg.
Infectious disease. Robbins pathologic
basic of disease. Cotran, Kumar, Robbins
5th edition WB Saunders company
London. 1994; 338-339.
2. RE. Condon. Dietmar H. Withmann.
Surgical infection. Peter J. Moris and
Ronall A. Malt . Oxford text book of
surgery. Oxford medical publication.
1994; 34-35.
3. A Cuschieri.H. Gilles. Specific infections of
surgical importance. In essential surgical
practice. A. cuschieri GR. Giles AR.
Moosa. Butterworth Heinam. Third
edition. 1995; 262-267.
4. Van Brien P. Mallelaer J. Ballist I. Fournier's
gangrene. Report of three cases and
review of the literature. Acta urologica
Balgica. [JC: 26y]. 1990; 58(2):161-70.
5. Lucca M. Unger AD. Deveuny AM.
Treatment of fournier's gangrene with
adjunctive hyperbaric oxygen. American
journal of emergency medicine. [JC:aa2].
Sep 1990; 8(5):385-7.
6. Tork L. Kozepessy L. Uraemic gangrene
syndrome. Acta dermato-venercologica.
[JC:Omg]. 1991; 71(5):455-7.
7. Cole HG. Neloon RL. Peters MS.
Pyoderma gangrenosum and
adrenocortical carcinoma cutis. [JC: dxb].
Sep 1989; 44(3):205-8.

The author :
Muhammad Shuja Tahir
FRCS (Ed), FCPS (Hon)
is professor and head of the
department of Surgery at
Independent Medical
College Faisalabad.
shuja@iu-hospital.com
SUMMARY
Gangrene ! Moist or wet gangrene
Etiology ! Gas gangrene
! Arterial obstruction ! Infective gangrene
! Infection ! Carbunci gangrene
! Trauma ! Meleney’s synergistic gangrene
! Venous obstruction ! Fournier’s gangrene
! Cancrum oris and noma vulvae
Types
! Dry gangrene

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