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M.

Shuja Tahir
Faisalabad, Pakistan IR-024
Surgery

GANGRENE
G angrene is the death (massive
necrosis) of macroscopic part of
the tissue with super-imposed
!
!
!
Streptococcal infection.
Bacteroides infection.
Mixed infection.
putrefaction.
TRAUMA
ETIOLOGY The injured tissue leads to loss of blood
It is caused by the tissue ischaemia supply and death of major part of distal
secondary to following conditions : tissue in following conditions ;
! Crush injuries.
ARTERIAL OBSTRUCTION ! Pressure sores.
Acute or chronic obstruction to the flow ! Circumferential burns.
of arterial blood leads to gangrene
formation. VENOUS OBSTRUCTION
The common diseases causing venous
The arterial obstruction occurs due to ; obstruction and gangrene are ;
! Atherosclerosis. ! Polycythemia.
! Thrombosis. ! Pancreatic neoplasms.
! Embolus (from atrial fibrillation). ! Trousseau's syndrome.
! Post diabetic neuropathic arteritis.
! Constriction ring of strangulated These may lead to peripheral venous
loops of bowel in volvulus and thrombosis which leads to retrograde
strangulated hernias. arterial obstruction and gangrene
! Buerger's disease (thrombo-angitis formation.
obliterans).
! Raynaud's disease. TYPES OF GANGRENE
! Cervical rib. Following clinical varieties of the
! Ergot poisoning. gangrene are seen ;
! Tourniquets, tight plaster and ! Dry gangrene.
bandages. ! Moist or wet gangrene.
! Intra arterial injection of ! Gas gangrene.
thiopentone or sclerosing ! Infective gangrene.
substances. ! Carbuncle.
! Meleney's synergistic gangrene.
INFECTION ! Fournier's gangrene.
The anaerobic infections may lead to ! Cancrum oris and noma
various types of gangrene. vulvae.
Following organisms commonly cause
2
the infections leading to gangrene ; DRY GANGRENE
! Clostridial infection. This is not true gangrene and should be
! Non clostridial anaerobic called mummification. There is massive
infection. necrosis but putrefaction is almost
! Staphylococcal infection. negligible. Although putrefactive

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organisms are present but their growth damaged muscles and foreign bodies.
and activity is very much limited. The local infection is associated with
liquefaction and gas formation.
The typical odor of gangrene is The common causative organisms are ;
minimal. This is due to slow and
progressive occlusion of the arteries ! Clostridium perfringens (cl.
supplying the gangrenous area. welchii).
! Clostridium Novyi (cl. oedema-
The gangrenous part is black, dry and tiens).
of the original shape. It is just mummi- ! Clostridium septicum.
fied. The line of demarcation is very
clear and separates the gangrenous Progressive putrefaction is caused by
area from healthy area eventually Cl. Sporogenies and Cl. histolyticum.
leading to auto-amputation.
The clostridia causing it produce potent
WET (MOIST) GANGRENE toxins such as ;
There is massive tissue necrosis and ! Hyaluronidase.
plenty of moisture. The putrefactive ! Collagenase.
organisms grow rapidly and are very ! Haemolysins.
active. ! Lecithinase.
! Other toxins.
The gangrene spreads rapidly. The
gangrenous area is black, swollen and It is a rare problem (0.1/100,000
3
smelly. The line of demarcation is not /annum) .
clear as the gangrene spreads rapidly.
There is large area of cellulitis at the It can follow an exogenous infection
junction of gangrenous area and from accidents, gun shot and other
healthy area. injuries leading to severe tissue
Toxaemia is very common in this type of damage with contamination, or
gangrene. Septic shock syndrome and endogenous infection from one's own
death of the patient may occur if not intestinal tract.
treated adequately and in time.
There is gross necrosis, putrefaction
This is usually secondary to sudden and gas formation.
occlusion of the arterial supply and
venous drainage. It also follows This is common after severe trauma,
infection and is associated with roadside accidents, high velocity
diseases such as diabetes mellitus. missile injuries, perineal injuries and
above knee amputations.
GAS GANGRENE
It is a life threatening condition. This It is characterized by profound toxemia,
occurs due to infection with gas- extensive local edema, massive
forming organisms. The infection with necrosis and variable degree of gas
gas forming clostridia causes. formation.

Myositis in the presence of dead or There is no fibrosis or leukocytic

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reaction. Gas gangrene is diagnosed clinically.
Dirty and infected wound is present with
The exotoxins produce cellulitis and lot of necrotic tissue and features of
progressive myonecrosis. These also septicaemia.
ferment muscle carbohydrates and
produce lactic acid and gas (H2CO2) On palpation there is crepitus at local
leading to fishy odor and greenish area.
black appearance.
Plain x-ray of the area shows presence
There is marked edema and enzymatic of gas in subcutaneous tissue in
necrosis of muscles commonly 24-72 patients with gas gangrene
hours after trauma.
SYNERGISTIC GANGRENE
Extensive exudate lacking in It is progressive gangrenous infection
inflammatory cells is present. The of the skin, fascia and areolar tissue2.
affected region is swollen and large
bullous vesicles are present on the skin It is progressive bacterial gangrene. It
which rupture. commonly involves skin and
subcutaneous tissue. It is caused by the
Inflammed muscles show massive synergistic action of micro-aerophilic
myonecrosis. The muscles are soft, non-haemolytic streptococci and
black, friable and semifluid due to anerobes.
action of proteolytic enzymes.
It occurs a week or two weeks after the
Gas bubbles are also present due to infection. It spreads very quickly unless
bacterial fermentation of the necrotic treated adequately.
tissue.
Burrowing ulcers (Meleny's ulcers) are
Microscopically there is myonecrosis, seen with gangrenous skin on the
extensive haemolysis and marked edges. There is gross necrosis of large
vascular injury with thrombosis. areas of skin. The necrosis of sub
cutaneous tissue extends far beyond
There is widespread formation of gas the gangrenous skin.
bubbles. The neuropathologic
1
changes are usually non specific . Non clostridial gas gangrenous
The mortality rate in treated patients cellulitis is usually caused by B.
varies between 25-40%. Untreated melaninogenicus and anaerobic
2
patients have almost always fatal end . streptococci.

Septic shock syndrome is also CANCRUM ORIS AND NOMA VULVAE


accompanied by haemolytic anaemia, These are types of infective gangrene of
renal failure and jaundice. muco-cutaneous junctions of mouth
and vulva.
End stage of gas gangrene may show
foamy liver and presence of gas These are seen in mal-nourished
bubbles in other viscera as well.

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children with infective lesions such as It presents as progressive papulo-
measles or chest infection pustular lesion or large necrotic sterile
ulcers.
There is slow necrosis of the tissue and
death may occur due to inhalation It follows systemic disorders such as
pneumonia. inflammatory bowel disease, rheu-
matoid arthritis, para-proteinemias,
FOURNIER'S GANGRENE haemotologic malignancies and other
It is a condition similar to synergistic malignant solid tumors.
gangrene. It is necrotizing fasciitis
spreading rapidly along facial planes, There is rapid improvement after
muscles, subcutaneous tissue and skin. treatment of the cause7.

There is subcutaneous edema. There is TREATMENT OF IMPENDING


dermal gangrene and appearance of GANGRENE
sero-sanguinous discharge. The causes leading to gangrene are
treated and blood supply of the area is
It occurs probably due to thrombosis of improved as soon as possible.
perforating vessels. The area involved
is usually scrotum, penis or both. Treatment of general diseases such as
diabetes mellitus, hypertension, atrial
Systemic toxicity may lead to septic fibrillation and peripheral ischaemia is
shock syndrome3. performed.

It is often associated with high Smoking should be stopped


morbidity and mortality. immediately.

Surgical debridement, broad spectrum The area at risk should be carefully


antibiotics and use of hyperbaric protected form minor trauma as well.
oxygen followed by plastic recons- Slight pressure by ill fitting shoes can be
tructive procedures are used to detrimental and may lead to gangrene
4,5
improve the survival of patients . formation.

URAEMIC GANGRENE SYNDROME Vasodilator drugs may be used for the


It is the cutaneous gangrene seen in improvement of local blood supply.
patients with chronic renal failure and
hyperparathyroidism. It is associated Sympathectomy whether surgical or
with vascular calcinosis and local chemical is helpful in the treatment of
ischaemia6. peripheral ischaemia.

PYODERMA GANGRENOSUM Anticoagulants can be used in


It is the infected cutaneous gangrene. gangrene secondary to thrombo-
It is a rare, recurrent and chronic embolic causes.
condition.

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

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

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

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