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58 Gangrene

Gangrene is the term used by the clinician to de­scribe local death of tissue (necrosis) occurring in the living body. Gangrene implies a fairly rapid process (developing in days) extending over a large visible area (a few to many centimeters) with an obvious inability of the tissues to repair or replace the gan­grenous part.

Although gangrene can occur in inter­nal organs (e.g., large intestine), it generally refers to a process occurring on the surface of the body. It may involve only the skin, or it may extend into deeper tissues such as muscle or nerves.

Gangrene may be either dry or moist. Dry gan­grene describes necrosis of the tissues of the extremi­ties resulting from vascular occlusion, such as occurs in severe arteriosclerosis of the legs. Wet or moist gangrene occurs when bacteria invades dead tissue, producing putrefaction. When the gas-forming group of bacteria is involved, gas gangrene occurs. A gan­grene may be dry at first, and be converted to the moist type by invading bacteria.

Clinical Manifestations

In dry gangrene, the arterial supply is gradually cut off and a drying or mummification of the tissues results. There is frequently an absence of inflamma­tion, but pain of varying degree may precede the color changes. The soft tissue slowly and progres­sively shrinks and the color gradually deepens until the whole area is coal black. Constitutional symp­toms may occur but are less severe than in moist gangrene.

Moist gangrene may be preceded by inflammation or trauma. The part is initially swollen and painful. The color is at first red then blue and finally turns to a green black. There is boggy swelling and putrid odor. If the moist gangrene is extensive, constitu­tional symptoms, such as fever, may be present.

A vivid description of hospital gangrene illus­trates well the clinical aspect of moist gangrene:

A wound attacked by gangrene in its most concentrated and active form presents a horrible aspect after the first forty-eight hours.

The whole surface has become of a dark- red color, of a ragged appearance, with blood partly coagu­lated, and apparently half putrid, adhering at every point. The edges are everted, the cuticle separating from half to three-fourths of an inch around, with a concentric circle of inflammation extending an inch or two beyond it; the limb is usually swollen for some distance, of a white, shining color, not peculiarly sensible except in spots, the whole of it being oedematous and pasty. The pain is burning and unbearable in the part itself, while the extension of the disease, generally in a circular direction, may be marked from hour to hour; so that in from another twenty-four to forty-eight hours nearly the whole of a calf of a leg, or the muscle of a buttock, or even the wall of the abdomen may disappear, leaving a deep great hollow or hiatus of the most destructive character, exhaling a peculiar stench which can never be mistaken, and spreading with a rapid­ity quite awful to contemplate. The great nerves and arter­ies appear to resist its influence longer than the muscular structures, but these at last yield; the largest nerves are destroyed, and the arteries give way, frequently closing the scene, after repeated hemorrhages, by one which proves the last solace of the unfortunate sufferer.... The joints offer little resistance; the capsular and synovial membranes are soon invaded, and the ends of the bones laid bare. The extension of this disease is in the first instance through the cellular structures. The skin is under­mined and falls in, or a painful red and soon black patch is perceived at some distance from the original mischief, preparatory to the whole becoming one mass of putridity, while the sufferings of the patient are extreme. (Buck 1902)

Etiology

Gangrene can have many causes; Table VIII.58.1 indicates the major ones. Some are now quite rare but at one time were common. Using this table as a guide, we shall discuss the various causes, highlight­ing those that have been of major consequence throughout recorded history.

Vascular Causes

Historically, ergotism resulted from ingesting rye bread contaminated by the fungus Claviceps purpu­rea. It led to a permanent decrease in the caliber of arterioles and, eventually, to dry gangrene of the fingers and toes and, less commonly, of the ears and nose. Ergotism was responsible for many epidemics of gangrene during the Middle Ages in Europe. Along with erysipelas it was known as St. Anthony’s fire. Although rare, ergotism may still occur today, as ergot preparations are often used in the treat­ment of migraine headaches.

Raynaud’s Syndrome. This syndrome is character­ized by marked episodic vascular spasms of the ex­tremities. During a typical attack, one or more digits initially turn white. After a few minutes, the color changes to a bluish red. Slowly, the normal color returns. These episodes are often triggered by cold or emotional stress. In severe cases, gangrene may en­sue, which is characteristically symmetrical and con-

Table VIII.58.1. Causes of gangrene

Vascular disease

Vascular spasm

Ergotism (St. Anthony’s fire)

Raynaud’s syndrome

Embolism

Arteriosclerosis

Organisms

Fat and gases

Dysproteinemias

Abnormalities of coagulation

Primary vascular disease (peripheral vascular disease) Arteriosclerosis

Thromboangiitis obliterans (Buerger’s disease) Diabetes

Vasculitis of the so-called collagen diseases

Rheumatoid arthritis

Systemic lupus erythematosus

Hypersensitivity to certain drugs

Physical agents

Bums

Cold

Trauma

Pressure

Ionizing radiation

Electrical bums

Chemical agents

Caustics

Venoms

Certain drugs

Coumadin

Heparin

Chemotherapeutic agents

Microbiological agents

Bacterial infections

Anthrax

Streptococci (necrotizing fasciitis, Fournier’s gangrene)

Mixed (postoperative synergistic gangrene)

Leprosy

Pseudomonas aeruginosa

Mycobacterial organisms (tuberculosis, Bumli ulcer) Viral infections

Herpes (simplex and zoster)

Smallpox

Chickenpox

Treponemal infections

Syphilis

Yaws

Bejel

Rickettsial infections

Rocky Mountain spotted fever

Typhus

Protozoal infections

Amebiasis cutis

Schistosomiasis cutis

Table VIΠ.58.1 (cont.)

Fungal infections

Histoplasmosis

Mucormycosis (phycomycosis)

ActinomycosisZnocardiosis

Cryptococcosis

Blastomycosis (North and South American)

fined to the fingers and toes.

It was once known as relapsing gangrene. Raynaud’s syndrome may occur alone {Raynaud’s disease) or in association with an­other condition usually of the collagen group of dis­eases {scleroderma, systemic lupus erythematosus, rheumatoid arthritis). It has also been seen as an occupational hazard in people who manipulate vibra­tory instruments such as jackhammers or chainsaws. Embolism. Embolism is the sudden occlusion of an artery by blood-borne particles. These may be atheromatous material dislodged from a vascular plaque upstream; vegetations from an infected heart valve; or other unusual particles such as fat (after extensive bony fractures), gas (decompression sick­ness), abnormal blood proteins (dysproteinemias), or blood clots. The acute vascular compromise can lead to gangrene of the extremities, usually of the dry type.

Arteriosclerosis. Arteriosclerosis may be an under­lying cause of embolism, and can also lead to grad­ual local vascular occlusion {thrombosis) of large and medium-sized arteries. It is common in the elderly and therefore has been called senile gangrene. A dry gangrene, it occurs mainly in the foot and was there­fore previously called Pott’s disease of the toe. It is generally preceded by severe pain and discomfort in the lower leg and foot. A special form of arterioscle­rosis is thromboangiitis obliterans or Buerger’s dis­ease. It commonly occurs in young and middle-aged men who are heavy smokers. Finally, diabetes can predispose to arteriosclerosis of smaller vessels with eventual gangrene of the feet and toes. Diabetic gan­grene is usually of the moist type. There are multi­ple other factors that may predispose to arterioscle­rosis. They include hereditary factors and general life-style habits such as overeating of animal fats, lack of exercise, and smoking. With recent changes in these habits and better control of diabetes, arterio­sclerosis and its resultant gangrene are now becom­ing less common. Surgical techniques are also avail­able for replacing or recanalizing occluded arteries of the legs, so that blood supply to the feet can be restored.

Physical Agents

Various types of injuries such as frostbite, compound bony fractures of the legs, contusions, gunshot wounds, and burns, if serious enough, may be the initial factor that triggers production of gangrene. However, this complication was more prevalent be­fore effective medical care became widely available.

Chemical Agents

Tissue can also be destroyed by chemicals either of exogenous or endogenous origin. Caustics such as carbolic acid (previously used as an antiseptic solu­tion) have been known to cause gangrene. Venoms of certain snakes (i.e., water moccasin), spiders (i.e., brown recluse spider), and jellyfish (i.e., Portuguese man-of-war) can cause local necrosis at the site of the sting or bite. Many chemotherapeutic agents (such as those used to treat malignancies) may also lead to local tissue destruction when they inadver­tently seep into the surrounding area during intrave­nous administration. Some systemically adminis­tered drugs may rarely cause gangrene (i.e., some anticoagulants such as coumadin).

Microbiological Agents

Many organisms produce a toxin that will directly cause cell death. Other toxins have vascular effects such as spasm or vasculitis. Some organisms pro­duce enzymes that can break down tissue locally. Other organisms - in particular, viruses - can di­rectly destroy cells by invasion. Only a few of the most important infections will be discussed here. Many can be found elsewhere in this work.

Various streptococci, including Streptococcus pyo­genes (group A beta hemolytic strep.), have been found to be the cause of certain varieties of gangrene. Of historical importance is hospital gangrene, also known as necrotizing fasciitis and pourriture des hδpitaux. This form of gangrene was the scourge of hospitals in the preantiseptic era. Today it is almost never seen. Trauma is usually the initiating factor, whereas predisposing factors are diabetes, alcohol­ism, and a generally debilitated state. Within 48 to 96 hours, gangrene would set into a wound and charac­teristically was rapidly progressive and deeply de­structive.

The patient would become febrile and even­tually succumb. Although some authorities feel that this type of gangrene was due solely to S. pyogenes, there is now more evidence to suggest that other organisms (alone or in combination) may give a simi-

Iar clinical picture. Another streptococcal gangrene, CaWedFourniersgangrene, is an acute gangrene local­ized to the scrotum. Finally, anaerobic streptococci in combination with other bacteria such as Staphylococ­cus aureus are the cause of postoperative synergistic gangrene. After a few days or weeks, gangrene devel­ops around an abdominal or thoracic surgical wound site. The process is rapidly progressive and may, if left untreated, lead to the death of the patient.

History and Geography

Ergotism has long been an important cause of cer­tain epidemics of gangrene in humankind. Gan­grene of the limbs has been recognized since ancient times, and a description of gangrene following trauma appears in Hippocrates. It is probable that gangrene in ancient Greece and Rome was due mainly to infections initiated by trauma of either accidental or military origin.

In temperate and Arctic zones of the world, cold injuries causing frostbite that led to gangrene have always occurred. Explorers of cold regions were of­ten affected, and gangrene produced by cold injury has also been a tremendous problem in troops en­gaged in wartime activities. Gangrene, for example, was quite prevalent among soldiers during Napoleon Bonaparte’s invasion of Russia. Yet frostbite was only one of the causes of gangrene associated with military activity. Trauma from penetrating wounds, contusion of soft tissues, and compound bony frac­tures were often the initial insult. The introduction of gunpowder in Europe in the sixteenth century produced a tremendous loss of life and limbs from gangrene that developed in these traumatic wounds. Poor hygienic conditions and overcrowding in hospi­tals led to epidemic wound infections. Because hospi­tal gangrene was rapidly progressive and lethal, many lives were lost, particularly during the Napole­onic Wars, the Crimean War, and the American Civil War. In many cases, there were almost as many soldiers killed from wounds and gangrene as were killed in action.

By the time of World War I, hospital gangrene was much less prevalent. The art of amputation and set­ting of fractures was advanced by the important contributions of such surgeons as Ambroise Pare in the sixteenth century, Pierre-Joseph Desault in the eighteenth, and John Bell at the turn of the nine­teenth, among others. Their work significantly con­tributed to decreased mortality from gangrene. The concept of antisepsis and asepsis was introduced in the late nineteenth century with the work of Louis Pasteur. This concept, when applied to management of wounds, is known as Listerism, in honor of Lord Joseph Lister, who was the first to recognize the value and clinical application of Pasteur’s discovery. Finally, the introduction of penicillin in the early 1940s totally eradicated hospital gangrene.

Arteriosclerosis is probably as old as humankind. Leonardo da Vinci, in the fifteenth century, illus­trated the arteries of a subject with senile arterio­sclerosis in one of his anatomic sketches. Along with prolonged life expectancy has come a greater susceptibility to degenerative diseases such as arte­riosclerosis and other vascular disorders. In the early nineteenth century, it gradually became clear that organic occlusion of the arteries could cause dry gangrene. Maurice Raynaud, in his now famous 1862 thesis, On Local Asphyxia and Symmetrical Gangrene of the Extremities, attempted to prove that there was a disease of the arterial system that might produce gangrene, but in which arterial oblit­eration was not present. Only recently have the roles of life-style, diabetes, and hypertension been recognized as contributing factors in the production of arteriosclerosis. Fortunately, widespread public education is now contributing to the decline of se­vere peripheral vascular disease and its associated gangrene.

In advanced countries of the world today, gangrene is much less common. Infectious gangrenes are easily treated or avoided by the appropriate antiinfective agents. However, there are now a growing number of individuals who are immunosuppressed from chemo­therapeutic agents and corticosteroids, which are used to prevent rejection in transplant patients, and to treat various cancers and autoimmune diseases such as rheumatoid arthritis. In such an immunocom­promised state, these patients are at increased risk of developing unusual infectious gangrenes whose etiologic agents may not be easily recognized or be readily treatable.

Diane Quintal and Robert Jackson

Bibliography

Brooks, Stewart. 1966. Civil war medicine. Springfield, Ill. Buck, Albert, ed. 1902. A reference handbook of the medi­cal sciences, Vol. IV, 300-8. New York.

Buerger, Leo. 1924. The circulatory disturbances of the extremities. Philadelphia.

1983. Thrombo-angiitis: A study of the vascular lesions leading to presenile spontaneous gangrene. American Journal OfMedical Sciences 266: 278—91. [Reprint of Buerger’s 1908 article in same journal.]

Enjalbert, Lise. 1978. De la pourriture d’hopital ⅛ !’infec­tion nosocomiale. Memoires de UAcademie des Sci­ences (Toulouse) 140: 67-73.

Moschella, Samuel L. 1969. The clinical significance of necrosis of the skin. Medical Clinic of North America 53: 259-74.

Tanner, J. R. 1987. St. Anthony’s fire, then and now: A case report and historical review. Canadian Journal of Surgery 30: 291—3.

U.S. Army. 1884. Index catalogue of the Library of the Surgeon-General’s Office. 1263-80.

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Source: Kiple Kenneth F. (Editor). The Cambridge World History of Human Disease. Cambridge University Press,1993. — 1200 p.. 1993

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