Chapter 135. Gas Gangrene and Other Clostridial Infections (Part 4) Gas Gangrene (Clostridial Myonecrosis) Gas gangrene is characterized by rapid and extensive necrosis of muscle accompanied by gas formation and systemic toxicity and occurs when bacteria invade healthy muscle from adjacent traumatized muscle or soft tissue. The infection originates in a wound contaminated with clostridia. Although >30% of deep wounds are infected with clostridia, the incidence of clostridial myonecrosis is quite low. These infections occur in both military and civilian settings. An essential factor in the genesis of gas gangrene appears to be trauma, particularly involving deep muscle laceration. The entity of clostridial myonecrosis is relatively uncommon after simple, through-and-through bullet wounds without shattering of bone and is relatively common after shrapnel fragmentation wounds, particularly when deep muscle is involved. In civilian cases, gas gangrene can follow trauma, surgery, or IM injection. The trauma need not be severe; however, the wound must be deep, necrotic, and without communication to the surface. Indeed, seeding of muscle tissue by C. septicum from a gastrointestinal source— often a malignancy—may lead to spontaneous nontraumatic clostridial myonecrosis (Fig. 135-1). The incubation period of gas gangrene is usually short: almost always <3 days and frequently <24 h. Some 80% of cases are caused by C. perfringens, while C. novyi, C. septicum, and C. histolyticum cause most of the remaining cases. Typically, gas gangrene begins with the sudden onset of pain in the region of the wound, which helps to differentiate it from spreading cellulitis. Once established, the pain increases steadily in severity but remains localized to the infected area and spreads only if the infection spreads. Soon after pain develops, local swelling and edema—accompanied by a thin, often hemorrhagic exudate—appear. Patients frequently develop marked tachycardia, but elevation in temperature may be only minimal. Gas usually is not obvious at this early stage and may be completely absent. Frothiness of the wound exudate may be noted. The skin is tense, white, often marbled with blue, and cooler than normal. The symptoms progress rapidly; swelling, edema, and toxemia increase, and a profuse serous discharge, which may have a peculiar sweetish smell, appears. Gram's staining of the wound exudate shows many gram-positive rods with relatively few inflammatory cells (Fig. 135- 1C). At surgery, muscle may appear pale because of the intensity of edema, but it does not contract when probed with a scalpel. When dissected, the muscle is beefy red and nonviable and can progress to become black, friable, and gangrenous. It is important to establish a diagnosis early, preferably by frozen- section biopsy of muscle. Despite hypotension, renal failure, and (often) body crepitation, patients with myonecrosis frequently have a heightened awareness of their surroundings until just before death, when they lapse into toxic delirium and coma. In untreated cases, as the local wounds progress, the skin becomes bronzed; bullae appear, become filled with dark red fluid, and are accompanied by dark patches of cutaneous gangrene. Gas appears in later phases but may not be as obvious as in anaerobic cellulitis. Jaundice is rare in wound gas gangrene (in contrast to uterine infections) and, when it does appear, is almost invariably associated with hemoglobinuria, hemoglobinemia, and septicemia. Cases of clostridial myonecrosis without a history of trauma have been reported. These patients have bullous lesions and crepitation of the skin; they present with a rapidly worsening course that includes myonecrosis, especially of the extremities. Bacteremia and Clostridial Sepsis The relatively common entity of transient clostridial bacteremia can arise in any hospitalized patient but is most common with a predisposing focus in the gastrointestinal tract, biliary tract, or uterus. Fever frequently resolves within 24– 48 h without therapy. Despite the finding of clostridial bacteremia following septic abortions and the frequent isolation of clostridia from the lochia, most of the patients involved do not have evidence of sepsis. In one series of 60 patients with clostridial bacteremia, half had an infected site that could be associated with the bacteremia, while the other half had a totally unrelated illness, such as tuberculous pneumonia, meningitis, or benign gastroenteritis. By the time blood culture reports are returned, patients frequently are completely well and sometimes have been discharged. Therefore, when a blood culture is positive for clostridia, the patient must be assessed clinically rather than simply treated on the basis of the culture result. Clostridial sepsis is an uncommon but almost invariably fatal illness following clostridial infection—primarily that of the uterus, colon, or biliary tract. This entity must be differentiated from transient clostridial bacteremia, which is much more common. C. perfringens causes the majority of cases of both sepsis and transient bacteremia. C. septicum, C. sordellii, and C. novyi account for most of the remainder of cases. C. sordellii sepsis with toxic shock syndrome has been associated with pregnancy and more recently with medically induced abortion. Clostridia account for 1–2.5% of all positive blood cultures in major hospital centers. The majority of cases of clostridial sepsis originate from the female genital tract and follow septic abortion. Introduction of a foreign body is a common antecedent event. In the uterus, residual necrotic fetal and placental tissues and traumatized endometrium may allow the growth of clostridia. Only a small fraction of cases of septic abortion (1%) are followed by serious sepsis. In these instances, sepsis, fever, and chills begin 1–3 days after the attempted abortion. The initial signs are malaise, headache, severe myalgias, abdominal pain, nausea, vomiting, and occasionally diarrhea. Frequently, a bloody or brown vaginal discharge is noted. Patients may rapidly develop oliguria, hypotension, jaundice, and hemoglobinuria. The hemolysis, which is secondary to C. perfringens α toxin, causes a characteristic bronzing of the skin. As in myonecrosis, the mental status of severely ill patients is characterized by increased alertness and apprehension. Local examination of the pelvis reveals foul cervical discharge, occasionally with gas. Frequently, laceration marks around the cervix or perforation of the cervical segment is evident. If the infection involves the myometrium or has spread to the adnexa, extreme tenderness, guarding, and an adnexal mass may be found. Laboratory studies in patients with sepsis reveal an elevated white blood cell count and may show pink, hemoglobin-tinged plasma. Anemia is proportional to the degree of hemolysis, and the hematocrit may be extremely low. Platelet counts may be reduced, and there is often evidence of disseminated intravascular coagulation (DIC). Oliguria or anuria, increasingly refractory hypotension, and hemorrhage and bruising may develop. Clostridia may enter the bloodstream from the gastrointestinal or biliary tract. This occurrence is associated with ulcerative lesions or obstruction of the small or large intestine, necrotic or infiltrating malignancy, bowel surgery, or various abdominal catastrophes. The patient may present with an acute febrile illness, with chills and fever but no other signs of localized infection. Intravascular hemolysis occurs in as many as half of such cases. Biliary or gastrointestinal symptoms, if present, may be the only clue to the etiology. Positive blood cultures provide the definitive clue to the diagnosis. Patients with malignant disease can also develop rapidly fatal clostridial sepsis, particularly from a gastrointestinal focus. The most common species in this setting is C. septicum. Characteristic signs and symptoms include fever, tachycardia, hypotension, abdominal pain or tenderness, nausea, vomiting, and (preterminally) coma. The tachycardia may be out of proportion to the fever. Only ~20–30% of patients develop hemolysis. A striking feature of this syndrome is the rapidity of death, which frequently occurs in <12 h. . Chapter 135. Gas Gangrene and Other Clostridial Infections (Part 4) Gas Gangrene (Clostridial Myonecrosis) Gas gangrene is characterized by rapid and extensive necrosis. clostridia, the incidence of clostridial myonecrosis is quite low. These infections occur in both military and civilian settings. An essential factor in the genesis of gas gangrene appears to be. by C. septicum from a gastrointestinal source— often a malignancy—may lead to spontaneous nontraumatic clostridial myonecrosis (Fig. 135- 1). The incubation period of gas gangrene is usually short: