Gangrene

Dr ADITYA
MBBS,MS (GEN.SURGERY)
• It is macroscopic death of tissue in situ (in continuity with
• adjacent viable tissue) with or without putrefaction.
• It can occur in sites like:
• Limbs
• Appendix
• Bowel
• Testes
• Gallbladder
• Causes
• Secondary to arterial occlusion like atherosclerosis, emboli,
• diabetes, TAO, Raynaud’s disease, ergots.
• Infective: Boil, carbuncle, gas gangrene, Fournier’s
• gangrene, cancrum oris.
• Traumatic: Direct, indirect.
• Physical: Burns, scalds, frostbite, chemicals, irradiat ion,
• electrical.
• Venous gangrene.
Clinical Features

• Colour changes: Pallor, greyish, purple, brownish black due to

disintegration of haemoglobin to sulphide.

• Absence of pulse, loss of sensation, loss of function.

• Line of demarcation between viable and dead tissue by a

band of hyperaemia and hyperaesthesia along with
development of a layer of granulation tissue.
TYPES OF GANGRENE
• DRY GANGRENE
• WET GANGRENE
• DIABETIC GANGRENE
• GAS GANGRENE
• MELENEYS GANGRENE
• CANCRUM ORIS
DRY GANGRENE
• Dry gangrene is due to slow, gradual loss of blood supply to
the part causing
• dry,
• desiccated,
• wrinkled,
• mummified part
• with proper line of demarcation from the viable adjacent
tissues
DRY GANGRENE
Wet gangrene
• is due to infection with putrefaction, causing oedematous,
• swollen,
• discoloured part,
• spreading proximally,
• with vague line of demarcation from the adjacent viable
tissues
WET GANGRENE
Differences between dry gangrene and wet gangrene

• Dry gangrene Wet gangrene (Moist)

• Clear line of demarcation is seen Line of demarcation is vague
• Dry, shriveled, mummified Oedmatous, putrified,
discoloured

• Slow, gradual loss of blood Sudden loss of blood supply

• supply
• Separation is by aseptic ulceration Septic ulceration causes
• separation.
• Limits to the demarcation Can extend proximally rapidly
• Causes are atherosclerosis, TAO Emboli, trauma are the causes
• Limited amputation is suffi cient Major higher amputation is
• often needed
• Investigations
• CBC,KFT, blood sugar.
• Arterial Doppler, angiogram (Seldinger technique).
• U/S abdomen to find out the status of aorta.
Treatment

• Limb saving methods:

• Drugs: Antibiotics, vasodilators, pentoxiphylline, praxilene,
• dipyridamole, small dose of aspirin, ticlopidine.
• Care of feet and toes:
• The part has to be kept dry.
• Any injury has to be avoided.
• Proper footwear is advised (Microcellular rubber footwear,
• MCR).
•
• Measures for pain relief is taken.
• Nutrition supplementation is done.
• The limb should not be warmed.
• Pressure areas has to be protected.
• Localised pus has to be drained.
• Cause is treated.
• Diabetes is controlled.
• Surgeries to improve the limb perfusion: Lumbar
sympathectomy,
• omentoplasty.
• Profundaplasty, femoropopliteal thrombectomy or
endarterectomy,
• arterial graft bypass are done according to the need.
• Life-saving procedures: Amputations may have to be done
• occasionally.
• Level of amputation is decided on skin changes, temperature,
• line of demarcation, Doppler study.
• Below-knee amputation is a better option as BK prosthesis
• can be fitted better and also the move ments of knee joint
• are retained. There is no need of external support and limp
• is absent.
•
• In above-knee amputation range of movements are less, limp
is present, and often requires third (stick) support to walk.
• Different amputations done are
• Ray amputation,
• below-knee amputation (Buerger’s amputation),
• Gritti-Stokes transgenial amputation,
• Above-knee amputation.
DIABETIC FOOT AND DIABETIC
GANGRENE

• Foot is a complex structure with many layers of muscles,

ligaments,
• joints, arches, fat, thick plantar fascia, vascular arches,
• neurological system which maintains weight-bearing, gravity,
• normal walk, stability and gait (swing and stance phases).
• Problems in diabetic foot
• Callosities, ulceration
• Abscess and cellulitis of foot
• Osteomyelitis of different bones of foot like metatarsals,
• cuneiforms, calcaneum
• Diabetic gangrene
• Arthritis of the joints
• Meggitt’s classifi cation of diabetic foot
• Grade 0: Foot symptoms like pain, only
• Grade 1: Superficial ulcers
• Grade 2: Deep ulcers
• Grade 3: Ulcer with bone involvement
• Grade 4: Forefoot gangrene
• Grade 5: Full foot gangrene
Pathogenesis of Diabetic Foot/Gangrene

• High glucose level in tissues is a good culture media for

bacteria. So infection is common.
• Diabetic microangiopathy causes blockade of microcirculation
leading to hypoxia.
Diabetic neuropathy:

• Due to sensory neuropathy, minor injuries are not noticed and

so infection occurs.
• Due to motor neuropathy, dysfunction of muscles, arches of
foot and joints occurs. And loss of reflexes of foot occurs
causing more prone for trauma and abscess.
• Due to autonomic neuropathy, skin will be dry, causing
defective skin barrier and so more
prone for infection.
 • Diabetic atherosclerosis itself reduces the blood supply and causes
gangrene.
• Increased glycosylated haemoglobin in blood causes defective
oxygen dissociation leading to more hypoxia. At tissue level there
will be increased glycosylated tissue proteins,
which prevents proper oxygen utilisation and so aggravates hypoxia.
• Clinical Features
• Pain in the foot.
• Ulceration.
• Absence of sensation.
• Absence of pulsations in the foot (Posterior tibial and
• dorsalis pedis arteries).
• Loss of joint movements.
• Abscess formation.
• Change in temperature and colour when gangrene sets in.
• Patient may succumb to keto acidosis, septicaemia or
myocardial infarction.
• Investigations
• Blood sugar, urine ketone bodies.
• Blood urea and serum creatinine.
• X-ray of part to look for osteomyelitis.
• Pus for culture and sensitivity.
• Doppler study of lower limb to assess arterial patency.
• Angiogram to look for proximal blockage.
• Ultrasound of abdomen to see the status of abdominal aorta.
• Glycosylated haemoglobin estimation.
• Treatment
• Foot can be saved only if there is good blood supply.
• Antibiotics—decided by pus C/S.
• Regular dressing.
• Drugs: Vasodilators, pentoxiphylline, dipyridamole, low
• dose aspirin.
• Diabetes is controlled by insulin only.
• Diet control, control of obesity.
• Surgical debridement of wound.
• Amputations of the gangrenous area. Level of amputation has
to be decided by skin changes and temperature changes or
Doppler study.
Care of feet in diabetic:

• – Any injury has to be avoided.

• – MCR footwears must be used (Microcellular
• rubber).
• – Feet has to be kept clean and dry, especially the toes
• and clefts.
• – Hyperkeratosis has to be avoided.
GAS GANGRENE
 ETIOLOGY
CAUSATIVE ORGANISM

1. Clostridium - welchi (60%)

2. Clostri dium - odematiens
3. Clostridium - septicum
4. Clostridium - histolyticus

SOURCE – Mainly Soil

PATHOGENESIS
•Clostridium organism cause infective gangrene by
involving mainly skeletal muscle.
•Low blood supply and low oxygen perfusion
 THE ORGANISM MULTIPLY TO
RELEASE TOXINS

NASELECITHIN HAEMOLYSIN HYALURONIDASE PROTEINASE

Haemolytic ,
membranolytic Extensive Rapid spread
Breaking protiens
and necrotic – haemolysi of gas
myositis. s

These will cause inflamation ,oedema ,necrosis & gangrene

of muscles.
1
7
 CLINICAL FEATURES
• Necrosis→septicaemia
• Crepitus felt due to gases
• Temperature – LOW GRADE
• Wound under tension–foul smelling discharge
• Khaki brown coloured skin due to haemolysis.
 CLINICAL TYPES

FULMINAN SINGLE SUBCUTANEOU

MASSIVE TYPE GROUP TYPE
T TYPE MUSCLE S TYPE
TYPE
• Rapid • Whole of • Extensors • One • Superficia
progress one limb of thigh single l
• Toxemia involved • Flexors of muscle
• Renal or liver leg
failure
 PROPHYLAXIS
• Proper wound cleaning
• Antibiotics i / v
• Minimum use of
tourniquet
• Gentle & effective p.O.P
• Anti gas gangrene serum.
 TREATMENT
• Excision of necrotic tissue &
muscle
• Proper antibiotic
• Blood transfusion.
• Hyperbaric oxygen.
 MELENEY’S GANGRENE
 Post –operative streptococcal or staphylococcal infection
 Involves skin of abdomen

TREATMENT – ANTIBIOTIC THERAPY

 CANCRUM ORIS /
NOVA

Infective gangrene of jaw, cheeks and lips

 ETIOLOGY PREDISPOSING FACTORS
• Fusiform bacillia • Malnourished
children
• Complication of
measles,kalaza
r
• Poor oral
hygiene
• Enteric fever.
 CLINICAL FEATURES
• Tooth infection
• Spreads to maxilla,mandible& then
soft tissue of the cheek.
• Oral mucosa ulcerated
• Tissue & bone is gangrenous
• Foul smell & purulent
discharge from mouth.
• Hole in the cheek.
• Unable to open mouth properly.
• Signs & symptoms of toxaemia.
 TREATMENT
• Antibiotic systemic
• Multivitamins
• Repeated antibiotic mouth wash
• Sequestomy in chronic Osteomyelitis of
mandible
• Plastic surgery of lip & soft tissue
THANK YOU