Gas Phlegmon

GAS PHLEGMON, EDEMA, bronze erysipelas, and gas gangrene are various manifestations of one and the same gas infection of a wound, which owes its development to the anaerobic Bacillus perfringens (Veillon) = Bacillus aerogenes capsulatus (Welch) = Bacillus phlegmonis emphysematosae (Frankel). This formidable infection is characterized by the development of gases in the tissues and necrosis, with or without the presence of inflammatory changes. It was first described by Velpeau, who observed it in 1839; Pirogov was the first to note the difference between gas phlegmon and gas gangrene. Before the war of 1914–18 and after it, gas phlegmon was usually observed in isolated cases, but there were sometimes small hospital epidemics; during the Imperialist War, it was encountered in large numbers (up to 300–450 cases according to individual authors). Gas phlegmon bears over 70 names [for example, gangrenous septicemia, traumatic (or septic) emphysema, gangrène foudroyante, acute gangrenous edema, acute mephitic septicemia (Pirogov), etc.]. Bacillus perfringens is a parasite in the intestines of humans and many animals. It is a non-motile rod without cilia, similar to the anthrax bacillus but with rounded ends; it is surrounded by what appears to be a capsule, forms very resistant spores (which withstand boiling) of an oval shape, and stains by the Gram method. The virulence of the gas phlegmon bacillus is related to its stage of development: the vegetative form is the most virulent, the sporogenic form the least. The bacillus is most often introduced into a wound by jagged fragments of artillery shells, ricocheting bullets, and other foreign bodies that carry with them particles of contaminated soil, as well as clothing, linen, and epidermis contaminated with the bacillus. According to studies by Fleming, soldiers' clothing is 83% contaminated with Bacillus perfringens. The infection is more often observed during positional warfare, when the soil is particularly contaminated with the excrement of troops. Clayey, poorly absorbent soil contributes more to infection than sandy soil. The gas gangrene bacillus can be found in 80% of gunshot wounds, but favorable conditions for its development (Fleming, Brailovsky), which usually begins near embedded foreign bodies, are far from always present. The infection therefore develops more easily in penetrating wounds. Wounds of the lower extremities are more often subject to infection by Bacillus perfringens, with wounds involving extensive damage to musculature that is saturated with hemorrhages, deprived of a fresh blood supply and oxygen access, and which represents a favorite soil for the development of the gas gangrene bacillus, being particularly favorable. Most often, the thigh in the upper third, buttocks, lower leg, foot, shoulder, etc., are affected (see separate table, figs. 1–4). In general, damage to tissues and their exsanguination contribute to the development of gas infection, which is sometimes observed even after subcutaneous injections of drugs and saline infusions. Outbreaks of previously latent infection were also observed after operations, as well as cases where the development of gas phlegmon bacilli was initially discovered far from the wound, at a site that had been subjected to prolonged pressure (e.g., during transport, tight bandaging, compression by clothing, etc.) and thus to relative exsanguination, which contributed to the development of bacilli already present in the blood at that site. Weak respiration and severe general exsanguination are favorable factors for the development of the infection. Bacillus perfringens, under suitable conditions, can penetrate into tissues from the gastrointestinal tract (for example, through the gallbladder). It is necessary to point out that to this day, no cases of infection of surgeons during operations or of personnel caring for patients have been known (Haberland), apparently due to the fact that bacilli entering well-nourished tissues and the blood in small quantities do not live longer than 3½–4 hours. This, of course, does not exclude the possibility of transmitting the infection to neighboring patients in a medical institution, which is why the isolation of patients affected by gas infection is recommended. The incubation period lasts from 2–3 hours to 23 days, on average 3–4 days. The bacilli of gas phlegmon, rapidly multiplying among crushed tissues deprived of sufficient nutrition, decompose proteins with the formation of gases, the speed of development and spread of which can serve as an indicator of the severity of the infection. The bacilli, multiplying, fill the connective tissue intermuscular spaces and lymphatic fissures, and penetrate between muscle bundles, fibers, and fibrils. The affected muscles perish throughout their entire length. The toxins released by the bacilli apparently affect the walls of blood vessels, which entails significant tissue edema. Larger vessels remain unaffected for longer. Hemolysis is observed; in the vessels, there are thrombi and stasis. The disruption of blood circulation and the influence of toxins lead to necrosis and decay of the infected area of tissue; the forming gas compresses the tissues and surviving vessels, which further worsens the blood circulation. Gas also appears in the vessels themselves. The development of gases is usually preceded by the appearance of multiplying bacilli in the tissue, which sometimes spread with enormous speed [up to 1 cm per minute! (Vincent and Stodel)]. Leukocytosis was observed more often in the blood, but leukopenia was also noted. With a pure Bacillus perfringens infection (gas gangrene), tissues usually do not produce a local inflammatory reaction (negative chemotaxis). If the infection is mixed (Bacillus perfringens and pyogenic microorganisms), then there are inflammatory phenomena in the tissues, sometimes with the formation of pus. Pyogenic aerobic microorganisms, on the one hand, facilitate the development of Bacterium perfringens by producing reducing substances, consuming tissue oxygen, and thereby creating anaerobic conditions; on the other hand, the inflammatory reaction, in the presence of pyogenic microorganisms, has some influence on the gas gangrene bacillus either through phagocytosis or because the cellular infiltration, filling the fissures, mechanically prevents the multiplying bacillus from penetrating into them (Pavlovsky), or, finally, because the gas gangrene bacillus is partially washed out of the fissures and the wound by the wound discharge present during inflammation. With more superficially located foci of infection, at the beginning of the disease, one can observe bronze-colored spots (of various shades) on the skin, sometimes with phlyctenas and vesicles, accompanied by pain, edema of the skin and subcutaneous tissue, and an increase in temperature—the so-called bronze erysipelas. In the subcutaneous tissue, one finds thrombosis of vessels and a bloody-serous exudate. Soon, sometimes after a few hours, at the site of a bronze spot left to itself, one can already find phenomena of necrosis with the development of gases, and in the vicinity, new bronze spots. Upon incision, it is found that the tissues are edematous, saturated with bloody or serous-purulent exudate and gases, with a cloying, putrid, unpleasant, sharp odor. A dirty-gray, sometimes liquid, sometimes thicker purulent discharge with gas bubbles comes from the wound. The muscles adjacent to the wound are sometimes saturated with gas bubbles for a long distance, are flaccid, tear easily, and are in various stages of necrosis and decay. The skin around the focus is edematous, tense, sometimes hyperemic, and over the focus, there are spots of various colors (bronze, dark brown, etc.) on it, sometimes subepidermal blisters with cloudy, brown, foul-smelling contents. There are phenomena of tissue emphysema. When shaving, a peculiar crackling-resonance is heard from the razor shaving the hair over the gas-saturated area, the so-called razor symptom (symptôme du rasoir). Upon percussion, there is tympanitis. Sometimes abscesses with foul-smelling gas-purulent contents form in the tissues. Nerves are compressed—hence the pain, sometimes twitching; later, with the death of the nerves and anemia, there is a loss of sensitivity, a feeling of numbness, heaviness in the affected area, and its cooling. The general condition is severe, but consciousness is preserved; temperature up to 39° and higher, chills, thirst, a frequent, initially full pulse, heaviness in the head, and restlessness. With the spread of the process, septic phenomena increase, the pulse becomes softer, the tongue becomes covered with a dark coating; delirium, yellowish discoloration of the skin, hiccups, vomiting. After 3–4 days, death occurs. In gas gangrene (pure Bacillus perfringens infection), which usually develops rapidly after a wound, the muscles are swollen, of a cloudy brown color (or other shades from pale gray, pale red to black), looking like boiled meat, and do not bleed upon incision (see separate table, fig. 2). If the development of gas predominates, the muscle is dry, brittle, friable, easily crushed between the fingers with a slight rustling (gas), and easily torn off in large pieces; in the presence of edema, it is flaccid, spreads, and tears. Upon pressure, a very scanty ichorous discharge with an abundant amount of bubbles of foul-smelling gas comes from the wound. The wound is gray, dirty, and dry. The skin is of a bronze-white, greenish-brown, gray-violet, or bluish-gray color and transitional shades, sharply tense, and edematous (see separate table, figs. 3, 4). Where there is less gas, the tissues closer to the wound are saturated with bloody exudate, and further away—with serous. Temperature up to 38–39° (not always elevated). The affected area is cold and devoid of all types of sensitivity. Local cooling spreads with the development of the process. There is a "razor symptom."

The general temperature drops rapidly, the pulse is small and frequent, pallor appears, a jaundiced skin coloration, cold sweat, restlessness, euphoria, then apathy, labored breathing, dry tongue, hiccups, consciousness is usually preserved; death sometimes occurs in the first 24 hours and even within a few hours in more severe cases, when one can watch the spread of the process by the hour. After death, the development of gas does not stop, due to which the corpses of those who died from gas infection bloat and decompose rapidly. Fig. 1. Skin lesion of the left thigh in gas phlegmon (after Fiolle). Fig. 2. Progress of gas phlegmon of the thigh with necrosis of the musculature (after Klieneberger). Fig. 3 and 4. Gas phlegmon of the thigh with involvement of the subcutaneous tissue (after Klieneberger-Nathanson). At autopsy, gas infiltration of the muscles and cellular tissue is found, sometimes gas in the internal organs (e.g., in the liver)—the so-called "foamy organs," fatty degeneration of the liver, heart, and kidneys; the spleen is usually not enlarged but is flabby. The veins contain hemolyzed blood mixed with gas bubbles; gas is also found in the heart. It is necessary to mention that sometimes gas in the veins was found even during life during operations (Maisonneuve, Pirogov, and others), and death from gas embolism was even observed (Schmidt). Novitsky and Minakov saw (fluoroscopy) the presence of gas in the inferior vena cava and the right heart 16 hours before death; an autopsy (35 minutes after death) confirmed the presence of gas (Sysoev). The appearance of gas in the blood is due to the penetration into the blood in weakened patients at the height of the process of Bac. perfringens in significant quantity, which was proven by blood cultures (Pavlovsky). Microscopically, in the affected tissues and organs, necrosis and disintegration of tissue elements with karyolysis and karyorrhexis are found; among the dead tissue, rounded voids (gas bubbles) are visible, surrounded by a large number of characteristic bacilli. Leukocytic infiltration is absent in pure cases. Early recognition of gas infection is not always easy. It is facilitated by increasing or sudden pain in the wound, edema, high temperature, and an accompanying odor. The diagnosis can be aided by the possibility, indicated by Krause, of determining gas in tissues using X-rays. If it is possible to perform a bacteriological examination, one can use Zacherl's medium (with Pyronin-Methylgreen), which, in the presence of Bac. perfringens, takes on an emerald-green color after just three hours. The Bethe test can help—a piece of diseased muscle does not sink in a 4-6% NaCl solution. A clinical picture similar to gas phlegmon can sometimes also be caused by the malignant edema bacillus, E. coli, and others. The prognosis is unfavorable. Mortality in the pre-antiseptic period was up to 90-100%. In the war of 1914-18, mortality fluctuated between 25 and 85% according to different authors and under different conditions (on average, about 50-55%). Usually, the prognosis is worse with an infection that develops rapidly after the injury. Rapid yellowish-bluish-grayish discoloration of the face indicates the malignancy of the infection, and in case of sudden jaundice (sharp hemolysis), the prognosis is absolutely unfavorable. Superficial, suprafascial forms are comparatively less dangerous; the prognosis is worse with involvement of the muscle-rich lower extremities, and especially when the process spreads to the trunk. Gas phlegmons have a somewhat better prognosis. The process can recur and produce metastases. Prevention of the introduction of infection—cleanliness of clothing, linen, and body—is far from always feasible, especially in combat conditions, when infection with Bac. perfringens is most frequent. It is necessary to pay special attention to the proper management of the wounded from the very first stages of providing aid. It is necessary to place the wound in the most favorable conditions possible for fighting infection: rest, elimination of compression of the wound area and adjacent parts (avoid tight bandages, tourniquets, etc.), wide opening of the wound, debridement with removal of dead musculature, bone fragments, stopping of bleeding, and drainage ensuring access of air to the wound. Where possible—primary excision of the wound. If the wounding foreign body is difficult to remove, it is better to leave it temporarily, limiting oneself to a wide opening of the wound. Avoid long transport; it is better to leave suspicious wounded in the nearest medical institutions, establishing careful supervision of the general condition and the wound area, and the odor from it. Various antiseptic substances for the wound are recommended—sublimate, iodoform, iodine, hydrogen peroxide, potassium permanganate, alum, zinc chloride, aniline dyes, Dakin's solution, hypertonic NaCl solution, etc. To increase local leukocytosis and obtain an inflammatory reaction in the vicinity of the focus, turpentine and camphor ether with turpentine were used. To neutralize the reducing substances produced in the gangrenous focus, oxygen was blown into the tissues, hydrogen peroxide was injected, etc., but without much success (there were several cases of embolism). Abroad, ignipuncture of diseased tissues was widely used (up to 600 punctures in individual cases). The listed measures are applicable at the beginning of the disease, when the process is limited to the area of the wound, provided there is preliminary surgical treatment of the wound (see above). With the increase of symptoms, wide incisions opening the affected layers to the borders of healthy tissues can help. With rapid spread of the process, as well as with an emerging threat of its transition from a limb to the trunk, one should not waste time on often fruitless attempts to stop the process with conservative measures, and timely amputation (exarticulation) within the borders of healthy tissues is necessary, if possible without a tourniquet. The wound is left open. In all methods of treatment, general measures are used to support the heart and the patient's strength. Serum treatment and vaccination are insufficiently developed.