Cellulitis most often occurs secondary to trauma of the skin with local inoculation of microorganisms, secondary to an underlying skin lesion or a postoperative wound infection, or by contiguous spread from a suppurative infection of other soft tissues or bone. However, cellulitis may also occur in the absence of any obvious local trauma. After inoculation of microorganisms into the subcutaneous tissues and skin, an acute inflammatory response is seen in the epidermis, dermis, adipose tissue, and superficial fascia, to different degrees.
The most common organisms causing classic cellulitis are Streptococcus pyogenes and S. aureus, with Streptococcus pneumoniae, other streptococci, and gram-negative bacilli encountered less frequently. Cellulitis due to gram-negative bacilli occurs primarily in immunosuppressed or granulocytopenic patients. A severe form of cellulitis may occur in individuals exposed to Aeromonas hydrophila in fresh water; the organism gains access through lacerations during swimming or wading. A severe and fulminant form of cellulitis that progresses rapidly to necrosis and bacteremia may be caused by Vibrio species, especially Vibrio vulnificus, acquired by exposure of a traumatic wound to salt water or raw seafood drippings.7
Classic cellulitis is characterized by erythema, pain, edema, and local tenderness involving an area of the skin with ill-defined borders. The area of initial cutaneous involvement expands rapidly. Occasionally there is lymphangitis and regional lymphadenopathy. Systemic manifestations include fever, malaise, and rigors. With untreated or rapidly progressive cellulitis, the process may spread to involve an entire extremity, producing severe systemic toxicity. Dehydration, mental apathy or obtundation, disseminated intravascular coagulopathy, respiratory failure, and septic shock may follow, necessitating intensive care management.
Appropriate laboratory diagnostic studies should be performed before antimicrobial therapy is begun. Any skin abrasions or draining sites should be swabbed for immediate Gram stain and culture. The stain is examined for the presence of organisms, their morphologic appearance, and the number and types of cells. Needle aspiration after injection of 0.5 mL of nonbacteriostatic saline into the leading edge of the cellulitis may be attempted; potential pathogens have been isolated in 10% to 38% of cases.8,9A combination of needle aspiration, skin biopsy, and blood cultures results in isolation of pathogens in approximately 25% of cases.10
For severe infections in which streptococci and staphylococci are considered possible, parenteral administration of a large-dose penicillinase-resistant penicillin (nafcillin or cloxacillin), 8 to 12 g/day in four or six divided doses, is most appropriate. Alternate agents include a first-generation cephalosporin, such as cefazolin (6 g/day in three divided doses), vancomycin (2 g/day in two divided doses), or clindamycin (1200 to 2400 mg/day in three divided doses). If the etiologic agent proves to be streptococcal, penicillin G should be substituted (6 to 12 million U/day). In the immunocompromised host or in the presence of a rapidly progressive cellulitis developing after a freshwater or saltwater injury, an aminoglycoside (gentamicin or tobramycin), 3 to 5 mg/kg in three or four divided doses or, alternatively, 5 to 7 mg/kg as a single daily dose, should also be administered.
Local care of cellulitis includes immobilization and elevation of the affected area. These measures are most appropriate when an extremity is affected. Analgesic drugs are administered as necessary. Cool compresses may help alleviate pain. The extent of the cellulitis should be outlined on the skin with an appropriate marker at the time of admission to facilitate objective daily assessments of the extent of spread. Frequent inspection of the involved area is necessary to detect any areas of crepitus or suppuration, which may require surgical drainage. Abscesses of the subcutaneous tissue are not infrequent after extensive cellulitis; judicious use of repeated needle aspiration may be necessary. Failure to achieve defervescence and a decrease in systemic toxicity within 48 to 72 hours after institution of appropriate antimicrobial therapy should arouse suspicion of suppuration or a more virulent soft tissue infection, such as necrotizing fasciitis or myonecrosis.
The term used for this type of cellulitis is not properly descriptive, but it persists because it is in common use. Other terms for this process include gas abscess, gangrenous cellulitis, localized gas gangrene, and epifascial gangrene. The process usually represents infection of already devitalized subcutaneous tissue without involvement of the deep fascia or underlying muscle. Microorganisms are introduced into the subcutaneous tissues from an operative or traumatic wound or from a pre-existing local infection. The subcutaneous tissues are devitalized owing to a local injury, an inadequately débrided wound, or a metabolic disturbance that compromises vascular supply (e.g., diabetes mellitus). Usually, the infectious process is not invasive but instead remains localized in the area of devitalized tissue.11,12 Extensive gas formation and suppuration, usually limited to the area of devitalized tissue, are present.
Anaerobic cellulitis may be clostridial or nonclostridial. Clostridium perfringens is the most commonly isolated clostridial species, followed by Clostridium septicum. Gram-negative rods, staphylococci, or streptococci are occasionally present but are not the predominant isolates. The nonclostridial form of anaerobic cellulitis is essentially the same process as clostridial cellulitis, but has a different microbiologic etiology. Obligate anaerobes are the predominant isolates, with Bacteroides fragilis, Bacteroides species, Peptostreptococcus, and Peptococcus encountered most frequently. Other bacteria that may be present include the gram-negative enteric bacilli (Escherichia coli and Klebsiella), staphylococci, and streptococci.
The clinical pictures of clostridial and nonclostridial anaerobic cellulitis are very similar and may be discussed together. Because this infection represents the local invasion of already devitalized tissue, the process does not generally have a virulent progressive course. The onset is gradual, with mild to moderate local pain and only mild to moderate tissue swelling. Constitutional symptoms are not prominent; the relative paucity of symptoms is helpful in distinguishing this entity from myonecrotic infections. A thin, dark, malodorous discharge from the wound or inoculation site, sometimes containing fat globules, with extensive and prominent gas formation, is characteristic. A dusky erythema may be present, and there may be extensive crepitus in the involved area. Although not initially invasive beyond the area of devitalized tissue, the condition must not be considered benign. If it is inadequately managed, the infection will eventually spread and lead to a rapid and extensive undermining of the skin similar to that seen in necrotizing fasciitis, with corresponding systemic toxicity.
A distinctive variant of gangrenous cellulitis was described and named by Meleney several decades ago.4 It has been called progressive bacterial synergistic gangrenepostoperative progressive gangrene, Meleney gangrene, and—if associated with burrowing necrotic tracts producing distant lesions—Meleney ulcer. The process usually begins postoperatively, particularly after abdominal or thoracic procedures, with a slowly developing shaggy ulcer with a gangrenous center surrounded by an inner zone of purple discoloration, which in turn is surrounded by an outer zone of erythema. Without treatment, the course is one of relentless indolent extension, but without significant systemic toxicity. Satellite lesions may occur; they represent tracts of burrowing subcutaneous infection that surface to produce a gangrenous ulcer on the skin. Pathologically, the process is usually limited to the upper third of the subcutaneous fat, but occasionally it extends down to fascia. The lesion was originally thought to be caused by a synergistic interaction between microaerophilic streptococci and S. aureus, but recently other microorganisms, including Proteus species and other gram-negative enteric bacilli, have been implicated.
Drainage from the wound or site of local injury should be sent for immediate Gram stain and culture. A simple method for obtaining anaerobic specimens for culture is to use a needle and syringe to aseptically aspirate the crepitant area at a site removed from the wound. All air should be carefully expressed from the syringe. If a swab is used, contact with normal flora should be avoided, and a commercial anaerobic transport medium should be used. Blood cultures should also be obtained. Radiologic examination should be performed to assess the presence and extent of soft tissue gas.
Initial antimicrobial selection is guided by the Gram stain of the purulent drainage. If only large “boxcar-shaped” gram-positive bacilli are present, the causative microorganism is Clostridium, and moderate to large doses of parenteral penicillin G (10 to 20 million U/day in six to eight divided doses) are indicated. If multiple organisms of different morphologies are present on the Gram stain, then one may assume that the process is polymicrobial, and an empirical broad-spectrum antimicrobial regimen should be instituted. An aminoglycoside (gentamicin or tobramycin, 3 to 5 mg/kg per day in three divided doses or, alternatively, 5 to 7 mg/kg as a single daily dose) and clindamycin (1200 to 2400 mg/day in three or four divided doses), with or without penicillin G (10 to 20 million U/day in six to eight divided doses), would be appropriate. In patients with impaired or changing renal function, a third-generation cephalosporin, such as cefotaxime, ceftriaxone, or ceftazidime, can be used instead of an aminoglycoside. Alternatively, a carbapenem such as imipenem or meropenem may be used as a single agent.
The major conditions to be differentiated from anaerobic cellulitis are necrotizing fasciitis and the myonecrotic syndromes.13 Distinguishing between clostridial myonecrosis and anaerobic cellulitis is necessary to avoid unnecessary extensive débridement. This distinction is made definitively at the time of surgery, which is mandatory to establish the diagnosis. The involved soft tissue must be laid open widely; devitalized tissue must be débrided; suppurative foci should be drained; and all involved fascial planes should be opened. The deep fascia and muscle must be carefully examined; if they are healthy, no further surgery is necessary. Further débridement may be necessary, depending on the amount of devitalized tissue present. The management of Meleney gangrene includes wide excision of the lesion plus antimicrobials as dictated by the culture results.
Necrotizing fasciitis is an uncommon but severe infection involving the subcutaneous tissue and the deep fascia. It spreads rapidly in the fascial cleft but spares the overlying skin until the later stages. Extensive undermining of the skin is the hallmark of this infection. It affects persons of all ages but is most common in middle-age and elderly adults. However, with the resurgence of group A streptococcal infections, including soft tissue infections, the incidence of necrotizing fasciitis in previously healthy young adults has increased.14,15 The infections may occur anywhere, but infections in the perineal region and in the extremities are most commonly reported.
The most common initiating injury leading to infection is minor trauma (∼80% of reported cases); operative wounds and decubitus ulcers account for most remaining cases. The presentation is usually acute or subacute, ranging from 3 to 14 days after the injury. In some cases, particularly those associated with group A streptococcus, the onset is very sudden; the condition may progress dramatically from a tiny abrasion to septic shock, with massive subcutaneous necrosis, within 24 hours.14,16 Many patients have underlying chronic illnesses,17,18 with diabetes present in 20% to 50% of patients, severe arteriosclerosis in 20% to 33%, and cardiovascular or renal disease in 50%. Nutritional status is also an important consideration, with marked obesity or marked wasting noted in many cases. With infection due to group A streptococcus, more than 50% of patients have no underlying illness and were previously in good health.
After the initial bacterial invasion, the infection spreads rapidly along fascial planes and subcutaneous fat, with ischemic tissue facilitating spread of the necrotizing process. At an early stage, histologic examination of full-thickness skin biopsies shows no abnormality. However, the subcutaneous fat and fascia show a contiguous nonspecific inflammatory reaction, with fibrinoid arteriolitis and thrombosis of vessels, and subsequent necrosis. If the condition is left untreated, the overlying skin becomes extensively necrotic because of thrombotic occlusion of the venules and arterioles supplying it.
It has been shown that traumatic surgical and vascular injuries generate areas of relative tissue anoxia, with the result that carbohydrate and protein metabolism proceed anaerobically, generating lactic acid. Buffer systems become depleted and acidosis develops, which causes lysosomal disruption and, hence, local autolysis and destruction. This environment provides an ideal milieu for anaerobic growth. Whether actual infection evolves is determined by several factors, including the means of inoculation and the size of the inoculum, altered host defense mechanisms, and the virulence of the bacteria. Altered host defenses play an important role in propagation of the infection. For example, high blood alcohol levels, steroids in large doses, and metabolic acidosis inhibit adherence of phagocytes, and patients with cirrhosis and metastatic carcinoma have poor phagocyte chemotaxis. The virulence of the bacteria is determined, to some extent, by their capacity to produce various enzymes (hemolysins, fibrinolysin, hyaluronidase, and collagenase). In addition, for S. pyogenes, the presence of M protein on the surface of the organism has an anticomplement effect and may function as a superantigen, leading to a massive release of potent vasoactive mediators such as tumor necrosis factor, interleukin 1, and myocardial depressant factor. The streptococcal pyrogenic exotoxins A, B, and C or other unknown antigens may also function as super-antigens and have been found to share DNA sequence homology with staphylococcal toxic shock syndrome toxin. Functioning as super-antigens, these toxins share the ability to mediate nonspecific binding to antigen-presenting macrophages and T-helper cells, leading to polyclonal activation of large numbers of these lymphocytes. The cytokine release associated with this activation is responsible for the severe toxic shock–like syndrome associated with S. pyogenes infections. Synergistic activity of different bacterial species has also been postulated on the basis of evidence from clinical experience and from experimental infections in animals.19 It is commonly assumed that aerobic organisms assist the growth of anaerobes by using oxygen, diminishing redox potential, and supplying catalase. Local ischemia and reduced host defense mechanisms in the presence of virulent pathogens combine to produce a milieu that is responsible for the alarmingly rapid spread (Fig. 55-2).
The pathogenic process in necrotizing fasciitis.
Necrotizing fasciitis may be due to a synergistic polymicrobial bacterial infection in which at least one anaerobic organism (usually a Bacteroides, Peptostreptococcus, or Peptococcus species) is isolated in combination with one or more facultative organisms (usually streptococci, E. coli, Klebsiella or Proteus species, or S. aureus),20 or it may be due to a single organism, usually S. pyogenes. In most cases of polymicrobial origin, multiple organisms are present, with an average of three or four isolates per patient. Some investigators distinguish acute group A streptococcal necrotizing fasciitis as a separate entity. Vibrio vulnificus and Aeromonas hydrophila have also been reported to cause a particularly virulent form of necrotizing fasciitis.
With necrotizing fasciitis, there is often a trivial injury followed, after several hours or days, by the onset of pain and swelling accompanied by chills and fever. The pain is progressive, relentless, and severe and is often out of proportion to the severity of the physical findings. There may be considerable pale erythema in the involved area; brown-to-bluish skin discoloration is not uncommon later in the course of the illness (Fig. 55-3). If the condition is left to progress, frank cutaneous gangrene may be seen. Pain is gradually replaced by numbness or analgesia as a result of compression and destruction of cutaneous nerves. Hypesthesia of the affected area may be a useful sign of the extensive undermining that occurs. Edema is present in most patients. Crepitation is not usual, but it may be found in patients seen later in the course of the illness. Fluid-filled vesicles may appear in the area of erythema, often quickly followed by frank cutaneous gangrene. If an exudate is present, it may be serosanguineous and foul smelling. Systemic toxicity with disorientation is often severe. Large extracellular fluid shifts, hypotension, shock, and jaundice may follow. When these findings are present in the setting of infection due to group A streptococci, the term streptococcal toxic shock syndrome is used.
Necrotizing fasciitis of the lower leg. Dusky erythema is present, with blistering and small patches of dermal gangrene.
A significant manifestation of necrotizing fasciitis is extensive undermining of the skin (Fig. 55-4) associated with necrosis of subcutaneous fat and deep fascia.21 The undermining can be demonstrated by passing a sterile instrument along the plane just superficial to the deep fascia (Fig. 55-5); the instrument cannot be passed with ordinary cellulitis.
Postoperative appearance of the lower leg presented in Fig. 55-3 All necrotic subcutaneous tissue was excised.
Necrotizing fasciitis with unopposed passage of a blunt instrument along the fascial cleft, indicating the characteristic undermining between the subcutaneous tissue and deep fascia.
Before antimicrobial therapy is started, samples for immediate Gram stain and for aerobic and anaerobic cultures should be obtained by direct needle aspiration of the involved area. Probing the lesion through an existing drainage site or through a small skin incision will reveal the characteristic undermining of skin seen in necrotizing fasciitis. The use of full-thickness skin biopsy with frozen section may aid the diagnosis.22
The principles of management include general supportive measures, administration of antimicrobial agents, and definitive surgery. General measures include the placement of central venous and arterial monitoring catheters, administration of intravenous fluids to correct dehydration, maintenance of adequate oxygenation, treatment of any underlying diseases (e.g., correction of ketoacidosis or congestive heart failure), and attention to the patient's nutritional needs. Total parenteral or enteral nutrition is required in the postoperative state to meet the dramatically increased nitrogen requirements associated with tissue repair, hyperthermia, sepsis, and vital organ requirements. Antibiotic selection should be guided by the initial Gram stain. In the absence of specific microbiologic data, broad-spectrum coverage should be given, including coverage for anaerobes, especially B. fragilis. An aminoglycoside (gentamicin or tobramycin), 3 to 5 mg/kg per day in three divided doses or, alternatively, 5 to 7 mg/kg as a single daily dose, plus clindamycin, 1200 to 2400 mg/day in three or four divided doses, is adequate initial therapy. If large gram-positive rods are noted, suggesting clostridia, or if group A streptococcus is suspected, penicillin G should be added (20 to 24 million U/day in divided doses). The combination of clindamycin and penicillin is considered the treatment of choice for severe soft tissue infection due to group A streptococcus. The addition of intravenous immunoglobulins, 0.4 g/kg per day for 4 to 5 days or 2 g/kg as a single dose with a repeat dose in 48 hours if the patient remains unstable, may be a useful adjunct for streptococcal toxic shock syndrome.23–25 In penicillin-allergic patients, chloramphenicol or metronidazole is useful as an alternative anaerobic agent. In patients whose renal function is impaired or rapidly changing owing to underlying disease or acute tubular necrosis, a third-generation cephalosporin, such as cefotaxime, ceftriaxone, or ceftazidime, can be used in place of the aminoglycoside. Alternatively, a carbapenem such as imipenem or meropenem may be used as a single agent.26
The mainstay of management is surgical exploration, débridement, and drainage, which should be done as soon as possible. Débridement and excision of all necrotic subcutaneous adipose tissue and fascia are required. The wound should be packed open. Daily exploration under general anesthesia is indicated for truncal or perirectal infections and for all patients who remain in a toxic condition. Frequent dressing changes are performed after suitable analgesia and are continued until healthy granulation tissue appears. Careful and regular reinspection of the wound is necessary because initial débridement is seldom complete, and small foci of infection and necrotic tissue often lead to further progression. It must be emphasized that conservative surgery leads to relapse of the process. In the pelvic and upper thigh regions, a hip disarticulation or hemipelvectomy may be required.
Mortality rate is extremely variable, ranging from 4% to 74%. High scores on the Acute Physiology and Chronic Health Evaluation on admission, age older than 50 years, diabetes, truncal disease, and failure to achieve adequate initial débridement are associated with high mortality rates.27
The bacterial myonecrotic syndromes involve bacterial invasion of previously undamaged healthy muscle, resulting in its rapid destruction. The process often referred to as gas gangrene is a fulminant, life-threatening infection for which early diagnosis and intervention are essential. Bacterial myonecrotic syndromes may be of clostridial or nonclostridial origin. Both entities have a similar pathogenesis, clinical presentation, and management.21 Clostridial myonecrosis occurs in the setting of muscle injury and concurrent inoculation with clostridial spores from the soil or a foreign body. Although most commonly encountered in penetrating war wounds, it is seen now in the following settings: (a) trauma, especially motor vehicle or agricultural accidents involving open fractures; (b) the postoperative period, especially after bowel or biliary surgery; (c) malignancy, especially colorectal tumors; (d) arterial insufficiency in an extremity; (e) septic abortion; (f) occasionally, burn wounds; and (g) rarely, after intravascular or intramuscular injections. Although colonization of a traumatic wound by clostridia is common, the frequency of clostridial myonecrosis is only about 1%. In an animal model, the minimal dose of C. perfringens required to produce a fatal infection is reduced by a factor of 106 when the organism is injected into devitalized, as opposed to normal, muscle. Clinically, however, clostridial myonecrosis does occasionally occur even in the absence of devitalized muscle. Once the clostridia begin to proliferate, several potent exotoxins are produced that have the capacity to destroy host tissue. At least 17 toxins are produced by C. perfringens, including α toxin, a phospholipase that disrupts cell membranes and results in hemolysis, platelet destruction, widespread capillary damage, and myofibril destruction. The μ toxin, a hyaluronidase, facilitates tissue spread and is thought to be responsible for the massive edema associated with this condition. As the process spreads, the involved muscle undergoes rapid destruction. Early pallor, edema, and loss of elasticity give way to a discolored, noncontractile muscle, which eventually becomes friable and disintegrates. The histologic findings are of coagulation necrosis.
Myonecrosis due to organisms other than clostridia has a pathogenesis not unlike that of necrotizing fasciitis. The infection may be introduced through a break in the skin, through intravenous injection of illicit drugs,28 a surgical wound or enterostomy, a decubitus ulcer, or a fistula. Predisposing factors include diabetes mellitus, obesity, advanced age, renal disease, and local trauma; diabetes mellitus is reported most commonly. With myonecrosis due to group A streptococci, no predisposing factors may be present. In drug addicts, infections of the extremities are more common, whereas perineal and buttock infections are more common in other populations.
When multiple microorganisms are responsible for myonecrosis, the facultative bacteria assist the growth of anaerobes by using available oxygen and destroying tissue (reducing the redox potential), which promotes a favorable milieu for the proliferation of anaerobic organisms. The process often involves muscle and fascia extensively, and it may secondarily involve areas of subcutaneous tissue and skin. It should be noted that necrotizing fasciitis will ultimately involve muscle, if left to progress.
Clostridium perfringens is the most common cause of clostridial myonecrosis, producing 80% to 95% of cases (Fig. 55-6). Clostridium novyi and Clostridium septicum are responsible for 5% to 20%, with other species implicated rarely. Nonclostridial myonecrosis is usually polymicrobial, although group A streptococcus may be a single causative agent. Most commonly, a mixture of facultative bacteria (E. coli, Klebsiella species, Enterobacter species, Proteus species, and S. aureus) and anaerobic bacteria (Bacteroides species, Peptostreptococcus species, and Peptococcus species) is found, an etiology similar to that seen in necrotizing fasciitis. Aeromonas hydrophila has also been described as causing severe myonecrosis after penetrating muscle injury in a freshwater environment.
Gram stain of Clostridium perfringens.
The incubation period of clostridial myonecrosis, from time of injury to appearance of symptoms, is usually 2 to 3 days, but it may be as brief as 6 hours. Intense pain, out of proportion to the extent of injury, is characteristic. The pain rapidly progresses in intensity and distribution. Fever is not present until later in the course. Within hours there appear signs of severe systemic toxicity: mental confusion, irritability, marked tachycardia, tachypnea, sweating, pallor, and hypotension. Delirium and stupor may supervene, although a period of intense mental alertness may occur before the onset of delirium. Renal failure, progressive hypotension and septic shock, intravascular hemolysis, and disseminated intravascular coagulopathy may ensue. Bacteremia occurs in only 10% to 15% of cases. Profound metabolic acidosis is common and can overwhelm compensatory hyperventilation, causing respiratory failure. Examination of the wound may initially show only tense edema and mild erythema. Later a spreading zone of woody edema appears, in addition to a characteristic bronzing of the skin. A thin, watery, brownish discharge with a sickly sweet odor may be present. Gas bubbles may be present in the discharge. Crepitus is usually present but is not a prominent feature. Tense blebs containing a thin serosanguineous fluid develop in the overlying skin, and areas of cutaneous necrosis appear in later stages. If an open wound is present, edematous muscle may herniate through the wound to the skin surface.
In nonclostridial myonecrosis, the process has its onset over several days. The port of entry is usually evident in the vicinity of the area of involvement. Moderate to severe pain and erythema, rather than edema, are more prominent. Progression is rapid, and systemic toxicity is severe; it may progress to shock and multisystem organ failure. Local crepitus may be present, as may a “dirty dishwater” discharge. Progression of the infection is rapid and may involve fascia and subcutaneous tissues. With infection due to group A streptococci, it is not uncommon to find myofasciitis and a toxic shock syndrome.
Early diagnosis is critical; its importance cannot be overemphasized. Confusion about the types of gas gangrene, failure to recognize that the infection does not have the usual signs of pyogenic inflammation, and failure to recognize that clostridial infections can develop without a history of recent trauma can create diagnostic difficulties. The major considerations are other gas-forming infections of the soft tissues, including anaerobic cellulitis and necrotizing fasciitis. The severe toxemia, limited crepitus, tense edema, and characteristic bronzing of the skin are suggestive, but not definitive, evidence of clostridial myonecrosis. Similarly, areas of cutaneous necrosis in a severely toxic patient with a “dirty dishwater” discharge suggest a nonclostridial myonecrosis. Adjunctive diagnostic tools include Gram stain and radiography. A Gram stain of the discharge or of soft tissue aspirate in clostridial myonecrosis reveals large, gram-positive bacilli with blunt ends, but few or no pus cells (which are destroyed by the clostridial lecithinase). A mixed flora or gram-positive cocci (streptococci) may be seen with nonclostridial myonecrosis. Precautions should be taken to ensure that anaerobic specimens are collected appropriately and transported promptly to the laboratory. A radiograph of the involved area may visualize gas that is not palpable and will give an indication of the distribution of such gas.
The principles of management include general supportive measures, antimicrobials, and surgery. Surgical exploration is definitive and is mandatory for the mere suspicion of clostridial or nonclostridial myonecrosis. Urgent surgical intervention is the ultimate diagnostic and therapeutic maneuver, and its importance cannot be overemphasized. Bacterial myonecrosis is characterized by a darkened, “cooked” appearance of the muscle, which does not contract on stimulation and bleeds very little on incision. Excision of involved muscles—or amputation, if necessary—and decompressive fasciotomies are the mainstays of surgical treatment. Any necrotic fascia or subcutaneous tissue should be débrided. General supportive therapy includes insertion of appropriate monitoring lines, administration of isotonic crystalloid to maintain blood pressure, maintenance of adequate oxygenation, correction of severe acidosis, and maintenance of electrolyte balance. Blood should be given sparingly during the acute stages if evidence of extensive hemolysis is present. Nutritional support is necessary in these critically ill patients, especially in the postoperative period.
For clostridial myonecrosis, the antimicrobial treatment of choice is large-dose penicillin G, 20 to 24 million U/day in six to eight divided doses. The dose must be reduced appropriately if a significant degree of renal failure is present. Chloramphenicol, 1 to 2 g/day in four divided doses, or metronidazole, 1 to 2 g/day in two to four divided doses, is a good alternative in the penicillin-allergic patient. If a mixed flora is found on Gram stain, the antimicrobial regimen should include an aminoglycoside (gentamicin or tobramycin), 3 to 5 mg/kg per day in three divided doses, or 5 to 7 mg/kg per day as a single daily dose, plus clindamycin, 1200 to 2400 mg/day in three to four divided doses. If clostridia are present on Gram stain, then penicillin should also be added to the regimen because some clostridia are resistant to clindamycin.29 If streptococcal myonecrosis or myofasciitis is suspected, the use of clindamycin plus penicillin is recommended. In addition, the use of intravenous immunoglobulin, as discussed in the previous section, may be a useful adjunct. A third-generation cephalosporin, such as cefotaxime, ceftriaxone, or ceftazidime, may be used in place of the aminoglycoside. A carbapenem such as imipenem or meropenem is a useful alternative as a single agent in nonclostridial myonecrosis.
Hyperbaric oxygen has been advocated as an adjunctive measure in patients with clostridial myonecrosis, but its role is controversial.30 Controlled trials have not been done and are unlikely to be done because of the limited number of cases that might be seen at a given institution and ethical considerations in the randomization of critically ill patients. Evidence supporting the use of hyperbaric oxygen comes from animal experiments, case reports, and uncontrolled small series. Its role at present appears to be in the management of selected patients with extensive involvement in whom extensive surgical débridement would be so mutilating as to threaten life or limb.