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GANGRENE OF EXTREMETIES

Presenter: Sheriff Abubakar Gaji & Muhammad

Abdullahi Ibrahim
Supervisor Dr. odongo james
OUTLINE
• Definitions: introduction
• Classification
• pathophysiology
• Causes
• Clinical presentation
• Patient approach
• Management
• Complications
GANGRENE
Definition:
• It is macroscopic death of tissue in situ with or without
putrefaction
Common Sites:
• Distal part of a limb
• Appendix
• A loop of small intestine
• Sometimes organs (gall bladder, pancreas or testis)
Etiology
Secondary to arterial obstruction:
• Thrombosis, Embolism (from heart in AF), Arteritis, Bueger’s disease, Raynaud’s disease,
ergotism, intra-arterial injections (thiopentone & cytotoxic substances)
Infective:
• Boils & carbuncle, gas gangrene, scrotum (fournier’s gangrene)
Traumatic:
• Direct injury (crushing injuries, bed sores)
• Indirect injury (vessel injuries).
Physical:
• Burns, scalds, frostbite, chemicals, irradiation, & electricity.
Neuropathic:
• Syringomyelia, leprosy.
Venous gangrene:
Due to extensive thrombosis in peripheral veins.
Clinical features
Gangrenous part lacks:
• Arterial pulsation
• Venous return
• Capillary response to pressure (no color
return)
• Sensation
• Warmth
• Function
Types Dry gangrene Moist gangrene
Site • Occurs in parts poor in tissue fluid and • Occurs in parts rich in tissue
exposed to dryness by evaporation. fluid & not exposed to dryness
by evaporation.
Examples • Senile gangrene of lower limb. • External genitalia, Internal
organs (lung, appendix,
intestine), lower limb (DM,
severe crush injuries).
Cause • Gradual slowing of blood-stream, as in • Sudden venous, arterial
atherosclerosis. occlusion by ligature or embolus,
and DM.
Infection • Minimal infection (aseptic ulcerative • Infection and putrefaction (septic
separation). ulcerative separation) are
present.
Pathology • Affected part is dry, wrinkled, dark in • Affected part is swollen, dark in
color (Hb disintegration), and greasy to color, edematous, offensive odor.
the touch. • Skin: tense, ulcerated, may show
• There is line of demarcation separate raised bleb (filled with gas
viable & dead tissue bubbles)
Separation of gangrene
Separation by demarcation:
• A zone of demarcation, between viable & dead tissue, appears first.
• It is indicated on the surface by a band of hyperaemia & hyperaesthesia.
• Separation is achieved by development of a layer of granulation tissue
forms between dead & living parts.
• These granulations extend into the dead tissue, until those which have
penetrated farthest are unable to derive adequate nourishment.
• Ulceration follows, and thus a final line of demarcation (separation)
forms which separates the gangrenous mass from healthy tissue.
• Types of Separation
• Separation by aseptic ulceration is seen in dry gangrene.
• Separation by septic ulceration is seen in infected condition and wet
gangrene.
Investigations
• Hemoglobin levels
• blood sugar
• Peripheral pulses – femoral popliteal dorsalis pedis post-tibial
• Wound culture
• Arterial Doppler, angiogram .
• U/S abdomen to find out the status of aorta.
Treatment of gangrene
Principles:
• A limb saving attitude
• Control arterial diseases: PTA, Bypass grafting
• Amputation: in crush, in spreading, and gas gangrene
• Control cardiac diseases (AF), treat anemia, and malnutrition.
• Control of Diabetes if present.
• Analgesia
• Affected limb should be kept dry (may use a fan)
• Protect pressure areas (heel, malleoli)
• Removal of crust to improve blood flow.
Varieties of gangrene
• Diabetic gangrene
• Direct traumatic gangrene
• Indirect traumatic gangrene
• Gangrene due to physical, chemical and
irradiation exposure.
• Gas gangrene
Diabetic gangrene
Diabetic gangrene: is due to three factors:
• Trophic changes resulting from peripheral neuritis
• Atheroma of the arteries resulting in ischaemia
• Excess of sugar in the tissues which lowers their resistance to infection.

• 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
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
Pathophysiology continued
• Diabetic atherosclerosis
• Itself reduces the blood supply and causes gangrene.
• Thrombosis can be precipitated by infection causing infective gangrene.
Blockage occurs at plantar, tibial, and dorsalis pedis vessels.
• Increased glycosylated haemoglobin in blood
• 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.
Clinical examinations and investigations include
• Blood sugar levels.
• Palpate for peripheral pulses: dorsalis pedis, posterior tibial, femoral,
and the absence of rest pain and intermittent claudication, imply that
there is no associated major arterial disease (atherosclerosis).
• A wound culture.
• A radiograph will reveal the extent of any osteomyelitis.
Treatment:
Control diabetes by diet, exercise and appropriate drugs. Use ABCs,
wound care, Amputation.
Direct traumatic gangrene
Direct traumatic gangrene is due to :
• local injuries e.g. crushes,
• pressure (as in the case of splints or plasters), or bedsores.
Bedsores (decubitus ulcers) are predisposed to by five factors:
• Pressure, Injury, Anaemia, malnutrition, moisture.
Bed sores can appear and extend with alarming rapidity in patients with disease or
injury of the spinal cord and other patients with debilitating illness.
Precautions about Bedsores include:
• Avoidance of pressure over the bony prominences (heel, malleoli, shoulders)
• Regular turning of patients and nursing on specially designed beds (Air beds),
which reduces the pressure to the skin.
• Skilled nursing (urinary incontinence).
Management of Bedsores
• Avoid erythema development
Once pressure sores develop, they are extremely
difficulty to heal, so
• Keep clean
• 2hourly tunning
• Debridement
• Hb should be maintained at normal levels.
• Excision of the dead tissue
• Flap pedicle skin grafting
Indirect traumatic gangrene
Indirect traumatic gangrene is due to interference with blood
vessels:
1. From pressure by a fractured bone in a limb, or by strangulation
2. Thrombosis of a large artery, following injury
3. Ligation of the main artery of a limb, as after division by injury
4. Poor technique for local anesthesia e.g. tourniquet + adrenaline-
containing local anesthetic solution leading to permanent occlusion
of all the arteries.
Treatment directed to the cause:
5. Fracture: closed or open reduction + direct arterial surgery for
damaged vessel + limb cooling.
6. If moist gangrene occurs and spreads rapidly, amputation may be
Physical and chemical causes of gangrene
May be due to:
• Frostbite
• Burns
• Chemicals
• Irradiations
• Electricity
Frostbite
Frostbite is due:
• To exposure to extreme cold, especially if accompanied by wind or
high altitudes (e.g. climbers and explorers).
• It is also encountered in the elderly or the vagrant during cold spells.
Pathologically, there is
• Damage to the vessel walls
• Edema.
• Severe burning pain in the affected part, after which it assumes a waxy
appearance and is painless.
• Blistering, and then gangrene, follows.
Treatment: Warming gradually, rest to limb, analgesics, conservative
amputation.
Trench foot
• Trench foot is due to cold, damp. and muscular
inactivity, and is predisposed to by tight clothing or ill-
fitting boots.
• Numbness is followed by pain, which is excruciating
when boots are removed. The skin is mottled like
marble, and in severe cases blisters containing blood-
stained serum develop, and moist gangrene follows.
• The pathology is similar to that of frostbite, and the
treatment is the same.
Injections
• Injection causes immediate and severe burning pain and
blanching of the hand.
• The needle should be left in position, and 5 ml of I per cent
procaine andior 2 percent papaverine sulphate injected to
obviate vascular spasm.
• Dilute heparin solution may also be given and if the needle is
in position.
• lntra-arterial thrombolysis intravenous low-molecular-weight
dextran may be employed.
• Brachial block must also be performed, and repeated if
necessary. Even so, gangrene of one or more fingers may
occur.
Drug abuse
• Arterial injection of drugs
• Femoral artery involved
• If pulses are absent, angiogram, intra-arterial
thrombolysis, heparin, dextran
• Recover with conservative treatment.
Ainhum
• Unknown aetiology.
• Usually affects black males (but some females) who
have run barefoot in childhood.
• Besides Central Africa, there are reports from Central
America and the East Asia.
• A fissure appears at the level of the interphalangeal
joint of a toe, usually the 5th, the fissure becomes a
fibrous band, which encircles the digit and causes
necrosis.
• The treatment is either early Z-plasty or, later
Ergot

• Common in Mediterranean Russians who eat rye


bread infected with Claviceps purpurea.
• Also occurs in migraine sufferers, who, for
prophylactic reasons, take ergot preparations
over a long period.
• The fingers, the nose and ears may be affected.
Gas gangrene

It is due to a bacterial infection:


• Clostridium perfringens, c. novyi, c. septicum, Which are anaerobes,
in soil, gut.
• Produce alpha toxins which are necrotizing and hemolytil.
• Common in war wounds, crush injuries.
Pathology:
• Myonecrosis, edema, thin pus, sweety odor (lysis of WBCs).
• Host immunity decreases.
Signs and symptoms:
• Sudden onset of pain, heaviness of limb, fever crepitus, tenderness,
tachycardia, hypotension, shock.
Gas gangrene

Investigations:
• Gram staining (gram + bacilli, no neutrophils),
• X-ray (gas in muscular plane),
• CT scan is 100% sensitive.
• Treatment:
• Antibiotics: penicillin G 10-24mUnits, clindamycin,
metronidazole.
• Hyperbaric oxygen therapy.
• ICU care
THANK YOU
References
• SRB manual of surgery
• Principles and practice of surgery 6th edition

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