Gangrene implies death with putrefaction of macroscopic portions of tissue. It is commonly seen affecting the distal part of a limb, the appendix or a loop of small intestine, and sometimes organs such as the gallbladder, the pancreas or the testis. Note that the term necrosis applies mainly to the death of groups of cells, although it is extended to include bone, i.e. a sequestrum. A slough is a piece of dead, soft tissue, e.g. skin, fascia or tendon.
Varieties of gangrene according to cause
Secondary to arterial obstruction from disease, for example:
• thrombosis of an atherosclerotic artery;
• embolus from the heart in atrial fibrillation or after coronary thrombosis;
• arteritis with neuropathy in diabetes;
• Buerger’s disease;
• arterial shutdown in Raynaud’s disease or ergotism;
• effect of intra-arterial injections — thiopentone and cytotoxic substances.
Infective: boils and carbuncles, gas gangrene, gangrene of the scrotum (Fournier’s gangrene).
Traumatic: direct, such as crushes, pressure sores and the constriction groove of strangulated bowel; or indirect, due to injury of vessels at some distance from the site of gangrene, e.g. pressure on the popliteal artery by the lower end of a fractured femur.
Physical, e.g. burns, scalds, frostbite, chemicals, irradiation and electricity.
Clinical features of gangrene
A gangrenous part lacks arterial pulsation, venous return, capillary response to pressure (colour return), sensation, warmth and function. The colour of the part changes through a variety of shades according to circumstances (pallor, dusky grey, mottled, purple) until finally taking on the characteristic dark brown, greenish black or black appearance, which is due to the disintegration of haemoglobin and the formation of iron sulphide.
Dry gangrene occurs when the tissues are desiccated by gradual slowing of the bloodstream; it is typically the result of atherosclerosis. The affected part becomes dry and wrinkled, discoloured from disintegration of haemoglobin and greasy to the touch.
Moist gangrene occurs when venous as well as arterial obstruction is present, when the artery is suddenly occluded, as by a ligature or embolus, and in diabetes. Infection and putrefaction are always present, the affected part becomes swollen and discoloured, and the epidermis may be raised in blebs. Crepitus may be palpated, owing to infection by gas-forming organisms. Moist gangrene is manifest also in such conditions as acute appendicitis and strangulated bowel.
Separation of gangrene
Separation by demarcation
A zone of demarcation between the truly viable and the dead or dying tissue appears first. It is indicated on the surface by a band of hyperaemia and hyperaesthesia. Separation is achieved by the development of a layer of granulation tissue which forms between the dead and the 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.
In dry gangrene, if the blood supply of the proximal tissues is adequate, the final line of demarcation appears in a matter of days and separation begins to take place neatly and with the minimum of infection (so-called separation by aseptic ulceration). Where bone is involved, complete separation takes longer than when soft tissues alone are affected, and the stump tends to be conical as the bone has a better blood supply than its coverings.
In moist gangrene, there is more infection and suppuration extends into the neighbouring living tissue, thereby causing the final line of demarcation to be more proximal than in dry gangrene (separation by septic ulceration). This is why dry gangrene must be kept as dry and aseptic as possible, and why every effort should be made to convert moist gangrene• into the dry type.
Vague demarcation; spread of gangrene; skipping and die-back. In many cases of gangrene from atherosclerosis and embolism, the line of final demarcation is very slow to form or does not develop. Unless the arterial supply to the living tissues can be improved forthwith, the gangrene will spread to adjacent tissues or toes, or will suddenly appear as ‘skip’ areas further up the limb. Signs of skipping should always be carefully looked for. Black patches suddenly appear, perhaps on the other side of the foot, on the heel, on the dorsum of the foot or even in the calf. Infection, another cause of the spread of gangrene, may spread upwards beyond the line of separation along the lymphatic vessels or cellular tissue into healthy parts; extensive inflammation then results. Except in diabetic gangrene without concomitant atherosclerotic obstruction, these forms of spread do not usually respond to efforts to save the limb and an above-knee amputation becomes necessary. To attempt local amputation in the phase of vague demarcation is to court failure, as gangrene reappears in the skin-flaps (‘die-back’).
Treatment of gangrene
A limb-saving attitude is needed in most cases of symptomatic gangrene affecting hands and feet. The surgeon is concerned with how much can be preserved or salvaged3. With arterial disease all depends upon there being a good blood supply to the limb above the gangrene, or whether a poor blood supply can be improved by such measures as percutaneous transluminal angioplasty or direct arterial surgery. A good or an improved blood supply indicates that a conservative excision is likely to be successful and a major amputation may be avoided. A life-saving amputation is required for a badly crushed limb, rapidly spreading symptomatic gangrene and gas gangrene.
General treatment includes that of cardiac failure, atrial fibrillation and anaemia, to improve the tissue oxygenation. A nutritious diet, essential in all forms of gangrene, and the control of diabetes, when present, are additional items of care. Pain, especially night pain, may be difficult to relieve. Nonaddictive drugs should be used whenever possible.
Care of the affected part includes keeping it absolutely dry. Exposure and the use of a fan may assist in the desiccation and may relieve pain. The limb must not be heated. Protection of local pressure areas, e.g. the skin of the heel or the malleoli, is required otherwise fresh patches of gangrene are likely to occur in these places. A bed-cradle, padded rings, foam blocks and air beds are useful preventive aids. Careful observation of a gangrenous part will show whether the lifting of a crust, or the removal of hard or desiccated skin, will assist in demarcation, the release of pus and the relief of pain.
Varieties of gangrene
Diabetic gangrene is due to three factors. These are:
• 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, including fungal infection.
The neuropathic factor impairs sensation and thus favours the neglect of minor injuries and infections, so that inflammation and damage to tissues are ignored. Muscular involvement is frequently accompanied by loss of reflexes and deformities. In some cases, the feet are splayed and deformed (neuropathic joints). Thick callosities develop on the sole and are the means whereby infection gains entry, often following amateur chiropody. Infection involving fascia, tendon and bone can spread proximally with speed via subfascial planes.
Clinical examination and investigations include those on the urine and blood for diabetes. Palpable dorsalis pedis and posterior tibial pulses, and the absence of rest pain and intermittent claudication, imply that there is no associated major arterial disease. A bacteriological examination is made of any pus. A radiograph may help to reveal the extent of any osteomyelitis.
Treatment. The diabetes must be brought under control by diet and appropriate drugs. The gangrene is treated along the lines already described, the accent being on conservatism if there is no major arterial obstruction. A rapid spread of infection requires drainage of the area by incision and the removal of any obviously dead tissue. This may often involve free and extensive laying open of infected tissue planes. Adequate surgical drainage of pus and the control of infection due to bacteria and fungi may then be followed by rapid healing. After healing, protection of the affected part is essential.
Direct traumatic gangrene
Direct traumatic gangrene is due to local injury and may arise as a result of crushes, pressure (as in the case of splints or plasters) or bedsores. Gangrene following severe injury, e.g. a street accident in which a vehicle passes over a limb, is of the moist variety and excision without delay is usually indicated. Amputation may be performed as close to the damaged part as will leave the most useful limb.
Bedsores (syn. decubitus ulcers) are predisposed to by five factors — pressure, injury, anaemia, malnutrition and moisture. They can appear and extend with alarming rapidity in patients with disease or injury of the spinal cord and other patients with debilitating illness. It is important to recognise patients at risk and take adequate prophylactic measures. These measures include the avoidance of pressure over the bony prominences, regular turning of patients and nursing on specially designed beds, which reduces the pressure to the skin. These beds include the high air loss Clinitron bed, low air loss Mediscus bed and the very low air loss OSA 1000. There are advantages in not blowing large quantities of air around the ward, and also advantages in being able to articulate the patient, yet removing the increased pressure and sheer forces produced by such articulation. Preventive measures are of the utmost importance. Thus pressure over bony prominences is counteracted by a 2-hourly change of posture and protection by foam blocks. A water bed or a ripple bed is sometimes desirable. Injury due to wrinkled draw-sheets and maceration of the skin by sweat, urine or pus is combated by skilled nursing and the use of an adhesive film such as Opsite.
A bedsore is to be expected if erythema appears which does not change colour on pressure. The part must be kept dry. An aerosol silicone spray may be used. Actual bedsores may be treated either by lotions or by exposure to keep them as dry as possible. Once pressure sores develop, they are extremely difficult to heal. They should be kept clean and débrided, and the use of rotation flaps should also be considered. The haemoglobin of the patient should be maintained at a normal level by transfusions of packed cells if needed. If the patient is young and otherwise healthy, excision of the dead tissue and flap pedicle skin grafting is often successful.
Indirect traumatic gangrene
Indirect traumatic gangrene is due to interference with blood vessels:
• from pressure by a fractured bone in a limb or by strangulation (strangulated hernia);
• thrombosis of a large artery following injury;
• ligation of the main artery of a limb, as after division by injury;
• poor technique for local digital anaesthesia. The combination of a tourniquet and an adrenaline-containing local anaesthetic solution can lead to permanent occlusion of all the arteries.
The likelihood of gangrene depends upon the sufficiency of the collateral circulation.
Treatment directed to the cause, e.g. closed or open reduction of a fracture together with direct arterial surgery for the damaged vessel, will usually prevent the onset of gangrene. The limb must be kept cool, so as to reduce metabolism to the minimum. When gangrene is slow to develop, a line of demarcation will indicate the level of vitality. If moist gangrene occurs and spreads rapidly, amputation may be needed to save the patient’s life.
Ergot, a cause of gangrene among dwellers on the shores of the Mediterranean Sea and the Russian steppes who eat rye bread infected with Claviceps purpurea, also occurs in migraine sufferers who, for prophylactic reasons, unwittingly take ergot preparations over a long period. The fingers, nose and ears may be affected.
Physical and chemical causes of gangrene
Frostbite is due to exposure to cold, especially if accompanied by wind or high altitude (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, which is followed by transudation and oedema. The sufferer notices severe burning pain in the affected part, after which it assumes a waxy appearance and is painless. Blistering and then gangrene follow.
Treatment.Frostbitten parts must be warmed very gradually. Any temperature higher than that of the body is detrimental. The part should be wrapped in cottonwool and kept at rest. Friction, e.g. rubbing with snow, may damage the already devitalised tissues. Warm drinks and
clothing are provided and powerful analgesics are required to relieve the pain which heralds the return of circulation. Paravertebral injection of the sympathetic chain may be helpful in relieving associated vasospasm. Amputations should be conservative. Hyperbaric oxygen may help.
Trench foot is due to cold, damp and muscular inactivity; it is predisposed to by tight clothing, such as garters, puttees and ill-fitting boots. Prophylaxis is of paramount importance. Numbness is followed by pain, which is excruciating when boots are removed. The skin is mottled like marble and, in severe cases, blisters containing bloodstained serum develop; moist gangrene follows. The pathology is similar to that of frostbite and the treatment is essentially the same.
Inadvertent intra-arterial injection of thiopentone can happen when a high division of the brachial artery results in one of its two terminal branches, usually the ulnar, passing superficially downwards in the antecubital fossa. The appreciation by palpation of pulsation of the vessel and of the withdrawal of bright red blood prior to injection should prevent this calamity. Injection causes immediate and severe burning pain, with blanching of the hand. The needle should be left in position, and 5 ml of I per cent procaine and/or 2 per cent papaverine sulphate injected to reduce vascular spasm. Dilute heparin solution may also be given intra-arterially if the needle is in position. Intra-arterial thrombolysis and intravenous low molecular weight dextran may be employed. Brachial block should also be performed and repeated as necessary. Even so, gangrene of one or more fingers may occur.
Drug abuse. Inadvertent arterial injection of drugs is becoming common in many countries with significant numbers of drug addicts. usually the femoral artery in the groin is involved, and presentation is with pain and mottling distally in the leg. Often all pulses down to ankle level are retained. If pulses have been lost, angiography and intra arterial thrombolysis may be considered (possibly with dextran and heparin in addition). If pulses are retained, dextran and heparin may be given but there is no firm evidence of their efficacy in this condition. Many cases are self-limiting and resolve spontaneously. It should be remembered that many of these patients carry the human immunodeficiency virus (HIV) or have frank acquired immunodeficiency syndrome (AIDS).
Chemical gangrene. Carbolic acid (phenol) is the most dangerous, as anaesthesia masks the pain which occurs before the onset of gangrene. Carbolic compresses should never be used, for fingers have been lost by application of compresses even as dilute as 1:80. The gangrene is due to local arterial spasm. In addition, there is danger of severe systemic effects from absorption of phenol. Local bicarbonate soaks should be applied. Later, excision of the slough and skin grafting are necessary.
Ainhum, a disease of 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. A fissure appears at the level of the interphalangeal joint of a toe, usually the fifth. This fissure becomes a fibrous band, which encircles the digit and causes necrosis. The treatment is either early Z-plasty or, later, amputation.
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