Surgical Management of Soft Tissue Infections

Surgical Management of Soft Tissue Infections

Symposium on Surgical Infections Surgical Management of Soft Tissue Infections Charles R. Baxter, M.D. * A variety of soft tissue infections may com...

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Symposium on Surgical Infections

Surgical Management of Soft Tissue Infections Charles R. Baxter, M.D. *

A variety of soft tissue infections may complicate traumatic injury or occur subsequent to either elective or emergency surgery and may require surgical treatment for successful management. The hallmarks of these "surgical infections" are the absence of the classical signs of local tissue inflammation, usually extensive involvement of soft tjssues, and the necessity of prompt, usually extensive, surgical therapy. Since many of these infections require urgent surgical treatment, familiarity with the presenting signs as well as awareness of the appropriate surgical therapy for each of these infections is useful in surgical practice. Successful management of the majority of these infections is dependent upon prompt diagnosis, usually by clinical signs alone. Early diagnosis is the key to successful management because mortality from infection as a general rule is time-dose related regardless of the offending organisms. Early diagnosis depends principally upon recognition of the characteristic clinical manifestations of the various surgical infections. Useful classification of surgical infections is difficult and, at best, incomplete. The majority of classifications are based either upon the type of organism or the "naming" of entities. Both are fraught with confusion. Identifying the infections according to the causative organism or combinations of organisms is the most complete but offers little to the rapid clinical diagnosis necessary to selecting appropriate management. Classification according to appropriate surgical therapy has been the most rewarding in obtaining prompt care and better ultimate survival with less morbidity. An attempt here is made to utilize this approach, limiting the entities discussed to those that are frequently encountered or that present special problems in recognition, differential diagnosis, or appropriate therapy. The infections are divided into those requiring extensive surgical incision and drainage and those requiring excision of tissue. The third grouping includes infections not requiring extensive surgical intervention but presenting problems in separation from the true surgical infections. This classification hopefully provides a broad reference system as an initial step in recognizing the spectrum within each group. Some of the specific problems within each of these three groups are discussed. ':'Professor, Department of Surgery, The University of Texas Southwestern Medical School, Dallas, Texas Surgical Clinics of North America- Vol. 52, No.6, December 1972

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SURGICAL LESIONS REQUIRING RADICAL INCISION AND DRAINAGE The main characteristic of the surgical infections which require extensive or radical incision and drainage is the involvement of principally a single tissue plane by the advancing infection. Each of these entities has fairly characteristic identifying signs in the pure state. Unfortunately, diagnosis of the surgical nature of these infections is delayed, most often because of partially effective antibacterial therapy which slows the rapid spread in the single tissue plane but does not alter local extension into both superficial and deep tissues. The late local signs often lead to "naming" an infection on the basis of the extensive deep tissue involvement instead of the true tissue plane origin of the infection. Naming such observations has led to considerable confusion in attempting to classify these infections. Acute Streptococcal Hemolytic Gangrene Necrotizing cellulitis, produced by a variety of strains of hemolytic streptococci, usually occurs on extremities following minor trauma such as puncture wounds, abrasions, or insect bites, and rarely, after operative procedures. Initially, the systemic response is less alarming than with erysipelas although a temperature of 100 to 102 F. and tachycardia are present. Chills are relatively infrequent. The affected skin region is hot, red, edematous, and often quite painful. Within 1 to 3 or 4 days after onset, and despite antibiotic treatment, areas of skin assume a dusky hue with the formation of blebs which contain dark, serous material (Fig. 1). Subsequently, the cutaneous gangrene may appear distal to the wound. 0

Figure 1. Acute hemolytic streptococcal gangrene, illustrating widely distributed blebs containing dark-reddish serous material.

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The mechanism producing skin gangrene is thought to be thrombosis of the blood vessels that supply the skin. This is questioned by some workers, however, because of the rapidity with which the gangrene may progress. Meleney!'·lo believes that it may be due to hyperallergic phenomena whereas McCafferty!' postulates that a proteolytic enzyme factor is responsible. Acute hemolytic streptococcal gangrene may be confused with several surgical infections producing cutaneous necrotizing lesions.u The fiery red, rapidly advancing borders of erysipelas which fail to respond dramatically to penicillin and develop bleb formation (initially seen near the origin of the wound) signify the surgical nature of the infection. More often, the edematous skin is a more dusky red, and is intensely swollen, and the enlarging blebs contain a reddish-brown odorless fluid. These characteristics, in the absence of crepitus, the absence of the musky odor of the dark fluid, and the presence of subdued wound pain, separate it from clostridial cellulitis. The length of time that the surgical illness has been clinically manifest and the extensive distribution and large size of the blebs serve to separate it from the late skin involvement of necrotizing fasciitis. In cutaneous hemolytic streptococcal gangrene, blister formation extends for long distances from the wound if the disease has been present for one or more days. In necrotizing fasciitis, skin involvement is late and is at first limited to the area immediately surrounding the wound although edema may extend for long distances from the origin of the infection. Treatment consists of emergency drainage with longitudinal incisions, thereby releasing skin tension and decreasing the ischemia. 1s The incision should extend beyond the obviously involved gangrenous and edematous areas. Undermining large skin flaps beneath the edematous area is usually not necessary. After incision and drainage down to and through the superficial fascia, the wound is treated by rest, elevation, and moist dressings which are frequently changed to aid in mechanical debridement. Infrequently, progressive gangrene occurs. Excision of these necrotic areas arrests the progression of cutaneous necrosis. Removal of areas of slough by sharp dissection is usually necessary after control of the infection.20 Before and after operation, antibiotic therapy, preferably with penicillin, should be given. No attempt should be made to wait for control of the infection by the antibiotic therapy prior to surgery. Important supportive care is limited to replacing the estimated edema fluid losses into the wound. Usually only 2 or 3 liters of balanced salt solution are required. Necrotizing Fasciitis Rapidly spreading necrosis of the superficial fascia is the most common of the surgical infections. It is equally likely to complicate either traumatic or surgical wounds. Of the operative wound infections, the majority occur when an abdominal hollow viscus has been entered. In either case, the highest incidence of these infections is seen in patients with ischemic small vessel disease, such as diabetics. Necrotizing fasciitis is often confused with acute hemolytic streptococcal gangrene and, indeed, there may be some overlapping.4 • 13. 20. 21

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Streptococci are prominent among the bacteria producing fascial necrosis and the skin involvement occurring in approximately 30 per cent of these patients is not unlike that seen in hemolytic streptococcal gangrene. A variety of organisms have been reported as the predominant cause of this infection. Meleny12 in his early series reported the streptococcus as the primary causative agent, while Wilson reported a preponderance of hemolytic staphylococci as the primary agent.22 Mead9 emphasized the necessary presence of gram-negative organisms, once thought to be laboratory contaminants, in addition to the presence of one of the gram-positive cocci. Wyrick and Rea14 reported an instance of mixed cultures in 68 per cent of 44 cases, and expressed the belief that inadequate culture procedures limited the documentation of the synergistic nature of this infection. In any event, the available data suggests that necrotizing fasciitis is a synergistic bacterial surgical infection, produced in most instances by a combination of a gram-positive coccus and a gram-negative rod. The gram-positive coccus may be a streptococcus, either aerobic or facultatively anaerobic, or a hemolytic staphylococcus in association with most frequently a pseudomonas, proteus, or enterobacter group organism. Other gram-negative rods are isolated much less frequently in these infections.a• 6. 7 The variety of flora capable of producing this type of infection emphasizes the need for accurate culture identification since antibiotic sensitivities may become important in the post-surgical antibiotic selection. The identifying clinical signs of necrotizing fasciitis are fascial dissection, hypoesthesia about the wound of origin, with minimal local pain and severe systemic toxicity of rather sudden onset (sudden, sustained high fever, tachycardia, anxiety or disorientation, often with acute severe hemolysis). Probing the wound edges with a blunt instrument results in easy dissection of the plane of the superficial fascia for some distance from the wound edge (Fig. 2). Little or no discomfort may be produced by this maneuver or by pin prick examination of the wound edge or the surrounding area. Lymphedema usually surrounds the wound and extends for some distance in one or more directions. Faint, mottled, reddish-purple skin discoloration is common, but extensive edema or serosanguinous skin blebs signify an advanced stage of the disease. Some cutaneous gangrene is present in approximately one third of the cases and signifies either an extremely rapid progression of the infection or more often inordinate time delays in diagnosis. These "late" cases have a poorer prognosis unless they represent partial containment by partially effective antibiotic administration. Systemically the patient is most often acutely ill with unrelenting fever rapidly rising from the 101 to 102 F. range to 103 to 104.5 F., with commensurate tachycardia, mild hypotension, agitated or confused mental state, and tachypnea. Evidence of red blood cell hemolysis may be present in the urine and often in the serum. Anemia and hypocalcemia are the consistent blood abnormalities. The primary therapy of necrotizing fasciitis is radical surgical incision and drainage of the wound beyond the outermost extent of the fas0

0

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Figure 2. Necrotizing fasciitis, showing unopposed dissection with an instrument in the plane of the superficial fascia.

cial involvement in all planes. Important to survival is close attention to details of physiologic repair, initial selection of antibiotics, and postoperative application of newer methods for early wound closure to eliminate as early as possible the stress of this severe complication in the course of the primary illness. Once the diagnosis is made from the clinical signs, preoperative management of fluids, electrolytes, and blood, as well as antibiotic selection, is important. Large quantities of extracellular fluid are trapped as edema in these extensive wounds. Often 4 to 6 liters of isotonic salt solution must be administered rapidly. Massive hemolysis occurs both in the wound and systemically, requiring several pints of blood (usually 1000 to 1500 ml.) during preoperative preparation. The necrosis of subcutaneous fat produces acute hypocalcemia, often as severe as that experienced in some cases of severe hemorrhagic pancreatitis. Large doses of calcium (5 to 10 gm.) must often be given during the first few hours of treatment. The multiple kinds of bacterial combinations potentially present indicate the need for a wide spectrum coverage, preferably intravenously to circumvent delays in absorption of intramuscular drugs in the volume depleted patient. An initial dose of 3 gm. of methicillin (Staphcillin) and 1 mg. per kg. of gentamicin (Garamycin) or 1.2 mg. per kg. of colistin (Coly-Mycin) intravenously are given and repeated at 4 hour intervals for the first 24 hours. These doses are then reduced to more ordinarily recommended doses postoperatively. An initial half gram of Kanamycin is administered intramuscularly and is followed by the same dose every 8 hours. Gastric dilatation and ileus are treated routinely with a nasogastric

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tube and hourly urine output is monitored by an indwelling urinary catheter. No more than 2 or 4 hours are consumed in initiating preoperative care prior to emergency surgery. Immediate operative treatment consists of radical and extensive incision past the areas of skin and subcutaneous involvement until good fascia is obtained (Fig. 3). As long as the fascia seems to give way to normal manipulations, the overyling skin and subcutaneous tissue must be incised. Not until stout normal fascia has been observed at all limits of the incision can the surgical treatment be considered adequate. Once these incisions have been performed, the wound should be pushed open and packed loosely with fine mesh gauze. Several multi-holed small catheters are placed in different portions of the wound for the constant delivery of a sterile aqueous solution containing 100 mg. of neomycin and 100 mg. of polymyxin B per liter of normal saline. Constant delivery of these solutions, maintaining a moist wound, should be continued until culture sensitivity studies dictate a more effective local antibacterial combination. The fine mesh gauze should be changed frequently during the first days after the surgical procedure. These dressing changes aid in debridement of the wound but more importantly permit examination of the wound edges for additional dissection of the fascia which is likely to occur and demand additional operative intervention. As soon as culture sensitivities are available, both local and systemic antibiotics are revised. Rapid bacteriologic control results and if secondary inoculation of the wound is prevented by careful surgical technique during dressing changes, the large open wound may be temporarily

Figure 3. Necrotizing fasciitis. Surgical incision beyond the extent of the fascial dis· section. Multi-holed soft catheters placed for postoperative administration of antibiotic solution.

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closed by fresh porcine heterografts which are changed at 1 to 3 day intervals until there is complete adherence of the biologic dressing. The porcine heterograft is used on the underneath surface of the large grafts since this represents a large area of the open surface. When the wound becomes sterile under the biologic cover, the large skin flaps may be replaced and any remaining open areas grafted with split-thickness skin grafts. The Tanner mesh graft is advantageous for covering these large wounds. Utilizing a 1: 1.5 expansion board, the holes in the interstices of the graft provide maximum drainage as well as better molding into the irregular contour of these wounds. Employing these principles of care, the current mortality rate is considerably lower than the previously reported 30 per cent reported from our institution. 14

Streptococcal Myositis This anaerobic streptococcal infection progresses more slowly than other streptococcal infections. 16 It is characterized by severe local pain, generalized toxemia, discoloration, edema, and crepitation of the muscle. A foul odor is generally apparent. There may be bleb formation and gangrene of the overlying skin. This infection usually occurs in closed wounds but may be a primary myositis. 1 The differentiation of streptococcal myositis from clostridial myositis is usually possible by the more pronounced cutaneous reaction in the former, the discolored but still viable muscle, the foul odor, and the presence of cocci by gram-negative smears of the fluid. Management consists of primary incision and drainage of the abscesses, fasciitis, and infected muscle groups. The supportive care and antibiotic of choice are the same as for other streptococcal infections. Occasionally, severely damaged or necrotic muscle requires limited excision. Clostridial Cellulitis Necrotizing cellulitis is produced by clostridial organisms and may be emphysematous (crepitant) or noncrepitant. A typical noncrepitant case following a puncture wound is shown in Figure 4. In either case, pain is usually the outstanding feature and may precede any significant local or systemic signs. Subsequently, small, flat fragile blebs extruding reddish-brown musky or foul smelling fluid precede frank necrosis of the skin and underlying subcutaneous tissues. Extensive edema of the affected part signifies the extent of the involvement. The systemic signs of infection characteristic of clostridial infection, extreme wound pain, tachycardia out of proportion to fever, and a toxic psychosis are indicative of the clostridial nature of the cellulitis. Therapy consists of extensive incision and drainage extending beyond the most proximal area of involvement into normal tissues. The areas of bleb formation represent necrotic material and should be excised at the time of the initial operative procedure. Sulfamylon is applied to the open wound which is then loosely dressed. The dressings are changed and Sulfamylon is re-applied at 12 hour intervals to obtain maximum effect of the local antibacterial therapy and to permit examination for additional extension which is common in this surgical infection.

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Figure 4. Clostridial cellulitis. Large blebs containing reddish-brown musky fluid adjacent to a puncture wound of the foot.

Tetracyclines, administered intravenously in large doses, both preoperatively and postoperatively, are the systemic antibiotics of choice. The mortality rate from clostridial cellulitis is extremely low in well managed cases as opposed to the continuing high mortality of clostridial myositis. The differentiation from acute streptococcal gangrene is cited above. When the infection is gas forming, differentiation from other gram-negative infections producing gas is simplified by the lack of systemic toxic effects, although extensive gas may be present in the tissue. Gram-Negative Anaerobic Cutaneous Gangrene A variety of anaerobic or microaerophilic gram-negative organisms, most often Bacteroides, may produce a severe, extensive but less rapidly spreading infection involving all tissue planes. These cases are often confused with necrotizing fasciitis,17 The unique characteristic of this infection is discrete large skin areas of bluish-gray necrosis separated by areas of normal skin (Fig. 5). A "dish water" fluid may form in some of the lesionsP The skin lesion overlies a much more extensive necrosis of subcutaneous tissue, fascia, and muscle (Fig. 6). Confluent liquefactive necrosis or dry gangrene is most often present in all of the fasciomuscle tissues underneath the areas of skin involvement. Extensive local necrosis is usually present before systemic manifestations are apparent. Systemically the patient may suddenly become gravely ill with tachycardia, fever, disorientation, and evidence of hemolysis. Gas-forming organisms may produce large quantities of dissecting air extending proximally, causing confusion with clostridial gangrene. However, tissue

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Figure 5. Gram-negative necrotizing cutaneous myositis. Typical bluish-gray skin lesions overlying extensive tissue necrosis (Bacteroides).

necrosis distant from the skin irivolvement is rare. The initial surgical treatment is incision and drainage of all involved tissues. The prominence of necrosis usually requires additional procedures or debridement. After the initial incision and drainage, the wound is loosely packed and soaked with the neomycin-polymyxin B solution described above, with frequent dressing changes and initiation of secondary debridement pro-

Figure 6. Gram-negative necrotizing cutaneous myositis. Extensive muscle necrosis underlying small area of cutaneous gangrene.

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cedures as necrosis indicates. Systemic antibacterial therapy usually includes tetracycline or chloromycetin (for Bacteroides) and kanamycin (Kantrex) for the possibility of other gram-negative organisms frequently present in these infections, which are often synergistic. About half of these surgical infections arise in the soft tissue of the extremity, while the other one half develop from abscesses of mixed gastrointestinal flora following perirectal abscesses, diverticular abscesses, and other infections arising from perforations or entries into the gastrointestinal tract.6 The lesion may also occur as a complication of ordinary infections originating peripherally.

SURGICAL INFECTIONS REQUIRING EXCISION OF TISSUE The surgical infections requiring excision of tissues are generally less fulminant (except for the clostridial infections) and tend to involve several types of tissue simultaneously. The most frequently encountered infections-gas gangrene and tetanus-are discussed elsewhere in this symposium. The remaining infections in this group are uncommon, but are important entities since they are highly lethal unless diagnosed early and aggressively treated. Particular attention is directed to the nonclostridial gas-forming infections which are the infections most commonly confused with the infections requiring radical excision of tissue. Progressive Bacterial Synergistic Gangrene This synergistic infection may arise as a complicating factor in the operative management of purulent infections of the peritoneal or pleural cavities or in association with traumatic wounds. It is produced by the synergistic action of a microaerophilic nonhemolytic streptococcus and an aerobic hemolytic staphylococcus or a gram-negative rod, most often Bacillus or Proteus. This infection is also known as postoperative progressive synergistic gangrene and Meleney's synergistic gangrene. The infection is typically recognized at 2 weeks following wounding. The skin surrounding the wound becomes edematous, red, and unusually tender. With progression, a characteristic lesion results that is demarcated into three zones (Fig. 7). There is a peripheral wide area of fiery red cellulitis around a zone of purplish tender skin. The central zone becomes necrotic and will ultimately ulcerate. The central ulceration results in undermining of the skin edges of the circumscribed lesion. Unlike other streptococcal infections, early systemic manifestations are impressive. A low grade fever is usually present, muscle wasting rapidly becomes prominent, and a profound anemia develops. The treatment of choice is radical excision of all necrotic layers, extending to an area well outside the involved borders (Fig. 8). Antibiotics assume a primary role before operation. Sufficient time for obtaining saturation of the patient obviates the devastating toxemia. Penicillin and broad spectrum antibiotics are given in high doses. Kanamycin (Kantrex) adequately covers the gram-negative rods occasionally isolated in the lesions. Following excision, the wound is allowed to remain open, covered by a loose gauze dressing for a few days. Heterografts or homo grafts are

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Figure 7. Bacterial synergistic gangrene. Central necrosis with undermining edges, a Figure 7. Bacterial gangrene. undermining edges, purple irregular border,synergistic and an outer zone of Central redness. necrosis Satellite with lesions surround the ulcer.a purple irregular border, and an outer zone of redness. Satellite lesions surround the ulcer.

Figure 8. Bacterial synergistic gangrene: Extensive excision of all tissue required for Figure 8. ofBacterial synergistic gangrene: Extensive excision of all tissue required for treatment lesion shown in Figure 7. treatment of lesion shown in Figure 7.

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usually applied after a few days when the base of the wound remains clean. Autografting procedures are carried out as soon as good adherence of the biologic dressing occurs. The mortality rate from this infection continues to be high owing principally to the delays in diagnosis and inadequate period of antibacterial coverage prior to surgery. Meleney's ulcer may be viewed as bacterial synergistic gangrene with the additional feature of burrowing necrotic tracts through various tissue planes resulting in multiple ulcerating lesions at distant skin sites. The causative organisms are the same as in bacterial synergistic gangrene but the clinical course is less severe and more protracted. This lesion is unusually rare today, occurring principally in debilitated or neglected patients. Treatment consists of excision of all the cutaneous ulcerations and excision of connecting tracts leaving the tissues open for local therapy. In extensive cases amputation may be necessary.

Non-Clostridial Gas-Producing Infections A variety of gram-negative organisms produce gas which may dissect tissue planes to great distances from the site of the primary infection. They present confusion in distinction from clostridial infections. In our experience these infections are much more common than gas gangrene. Escherichia coli and Aerobacter aerogenes, anaerobic streptococci, and· several species of Bacteroides are included in the gas-producers responsible for this deceptive state. The typical patient is one who develops wet gangrene of a toe or foot ulceration with proximal cellulitis and edema. Air is detected in the proximal tissues by x-ray or physical examination. The correct diagnosis is suggested by the lack of systemic toxicity accompanying such extensive tissue involvement. Therapy consists of local wound management only, ignoring the tissue involvement by the gas dissection. Needless amputations of extremities or other radical procedures are thereby avoided. Non-Clostridial Myositis Rapidly advancing necrotizing myositis caused by a variety of gramnegative organisms may complicate extensive soft tissue wounds. Initial surgical debridement has usually been inadequate. These infections occur most frequently with compound long bone fractures or perineal injuries. A much less virulent spontaneous bacterial myositis is extremely rare. 1 The typical acute onset of tachycardia, fever, disorientation, hemolysis, and wound edge necrosis heralds the onset of advancing muscle necrosis. Surgical intervention, removing all nonviable muscle tissue beneath the necessary extensive skin flaps offers control of the infection. Cultures of the wound are most important for the proper selection of antibiotic care. Amputation is frequently preferred when local tissue necrosis is too extensive to permit limb salvage. Human Bite Infections Reasonable and adequate initial care is most effective in the prevention of this type of infection. Adequate excision of the wound as soon as

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the patient is seen, followed by copious irrigation with sterile saline solution, is the treatment of choice. In only rare instances should bite lesions be sutured. Immobilization and antibiotic therapy, usually penicillin, are necessary adjuncts. If the original wound is treated inadequately, inflammation appears rapidly, usually within the first 48 hours. If the wound has been closed it should be immediately opened. The infection is almost always polymicrobic, consisting of spirochetes, staphylococci, anaerobic streptococci, aerobic nonhemolytic streptococci, and gram-negative rods. When the infection is established, radical debridement, principally excision of the infected area, must be performed.

NON OPERATIVE INFECTIONS It will readily be recognized that the majority of these infections do not require surgery in their initial management. Some are characterized by the familiar classical signs of local inflammation-redness, heat, pain, and edema. Although placed in the nonsurgical category, it is understood that when signs of inflammation occur in closed wounds (sutured or puncture-type wounds), opening of such wounds is mandatory as primary therapy. Several entities chosen for brief discussion in this group are those presenting special problems in recognition or confusion with "surgical" infections requiring radical surgery for initial therapy.

Erysipelas The one time common, fiery red, elevated lesion of erysipelas with its irregular, well demarcated, rapidly advancing border is infrequent today. It is an easily recognized lesion caused by the Group A hemolytic streptococcus. The major problem that erysipelas presents is in differentiation from acute hemolytic streptococcal cutaneous gangrene which is caused by the microanaerobic streptococcus. Early in its course, streptococcal cutaneous gangrene may appear as erysipelas but the rapid appearance of blisters containing a reddishpurple, odorless fluid, and continued advancement of the irregular border despite penicillin therapy lead to the diagnosis. A second surgically important feature of erysipelas is the occurrence of secondary abscesses in regional lymph nodes after successful treatment of the primary skin lesion. These secondary complications may occur as groin or retroperitoneal abscesses or, rarely, as mediastinal abscesses several weeks following the successful management of the original infection. Lymphangitis and Lymphadenitis Suppurative lymphadenitis or lymphangitis may occur as a complication to any infection process which results in the obstruction or obliteration of larger numbers of lymphatics. Recurrent bouts of pustular lesions may appear distal to an area of lymphatic destruction from weeks to years after a variety of surgical infections. Such lesions are frequently encountered after necrotizing fasciitis, suppurative thrombophlebitis, or congenital lymphatic obstruc-

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tions (Milroy's disease). Culture of these multiple pustules may reveal staphylococcal organisms but often cultures are persistently negative. It is likely that in the latter group, the organism is an anaerobic organism of L-form 2 which cannot easily be isolated. Successful treatment of an acute episode of the staphylococcal lesion is obtained with appropriate antibiotics, daily hexachlorophene baths, and incision and drainage of the persistent pustules. Antibiotic therapy is chosen by culture-sensitivity studies. When the cultures are persistently negative, tetracycline in dosages of 1 to 2 gm. per day is almost always effective. Permanent cure (Le., prevention) is best obtained by prophylactic intermittent courses of low doses (500 mg. per day) of tetracycline for 2 week periods for 6 to 9 months. The empiric approach outlined above is less than scientifically desirable, but is usually successful. In all instances, the initial work up includes a search for dysgammaglobulinemia, collagen disease, chronic hepatitis, peripheral vascular diseases, and allergies. 19 Sporotrichosis represents a specific cause of subacute ulcerative lymphadenitis which is often confused with bacterial synergistic gangrene. An innocuous wound of the extremity evolving to chronic ulceration with progressive suppurative involvement of proximal lymph nodes is characteristic of the disease. The patient with extensive involvement of an extremity appears healthy, as opposed to the cachetic, febrile patient with bacterial gangrene. Systemic toxicity with sporotrichosis suggests pulmonary or bone involvement. The typical lesions of sporotrichosis are shown in Figure 9. This 17 year old boy's illness began with an abrasion on the forearm during football practice. It became "infected" and an undulant ulceration developed at the contact point. Multiple courses of antibiotics produced drug fever,

Figure 9. Sporotrichosis. Multiple ulcerative lesions following lymph node distribution. Often confused with bacterial synergistic gangrene.

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rashes, a 40 lb. weight loss, and three hospitalizations extending over a 3 month period and costing over $8,000. Approximately half of cases of sporotrichosis stem from skin breaks in contact with fertilizer containing the fungus. Athletes with abrasions during workouts are common examples. Since the history does not suggest etiology of the infection, the patient is subjected to extensive inappropriate confusing therapy while the disease continues unabated. Treatment with 15 qt. of a saturated solution of potassium iodide (SSKI) ti.d. for 2 to 6 weeks results in complete healing.

Purpura Fulminans Rapidly coalescing purpuric skin lesions distributed over the entire body are characteristic of the disseminated intravascular coagulation associated with pneumococcal or meningococcal infections or following in the wake of bacterial, viral, or rickettsial diseases. These once lethal infections are currently remediable diseases producing a problem in wound care, diagnosis and management for the surgeon in increasing numbers. The irregular splotchy blue skin lesions appear at first to be limited to the more superficial layers of the skin. Early recognition of the cutaneous purpura and prompt initiation of heparin therapy prevents progressive skin destruction. As with other clinically significant disseminated intravascular coagulation states, complete anticoagulation often requires initial large doses of heparin in order to achieve prolongation of the clotting time to the desired 2 to 3 times normal. When diagnosis is delayed for 1 to 2 days, the skin necrosis increases in depth, and a full-thickness injury that requires grafting results. The management of these sterile necrotic areas should be conservative, utilizing topical antibacterial creams such as Sulfamylon or silver sul-

Figure 10. Purpura fulrninans. Dry gangrene of the toes and fore-feet and full-thickness necrosis of skin over 40 per cent of the body surface.

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fadiazine until all necrotic areas are clearly demarcated. Excision and grafting can then be accomplished. Alternately, debridement of the eschar can be done slowly, but this results in a less satisfactory cosmetic result. Often, delays in diagnosis result in swelling of underlying muscle, necessitating extensive fasciotomies to preserve the viability of the distal portions of the extremities. Failure to appreciate the ischemic necrosis produced by swelling may necessitate late amputation of one or more extremities. Such an example is seen in Figure 10. Bilateral fore-foot amputations and extensive debridement of the lateral and medial compartments of both lower legs were necessary.

SUMMARY Severe soft tissue infections are infrequent, but demand prompt recognition of their clinical signs to insure rapid surgical treatment. Basing a classification of these infections on the type of surgical care required by each infectious entity, offers the most satisfactory approach to these varied disease states. The infections are divided into those requiring no radical surgery, extensive incision and drainage, or primarily excision of tissue. The principles of care of the most frequent and most highly lethal infectious entities, as well as the infectious lesion causing confusion in diagnosis, are discussed.

REFERENCES 1. Altrocchi, P. H.: Spontaneous bacterial myositis. J.A.M.A., 217:819, 1971. 2. Altemier, W. A., Hill, E. 0., and Fuller, W. D.: Acute and recurrent thromboembolic disease: A new concept of etiology. Ann. Surg., 170:547, 1969. 3. Andrews, E. C., and Cruz, A. B., Jr.: Necrotizing fasciitis: diagnosis and treatment. Texas Med., 65:50, 1969. 4. Crosthwait, R. W., Jr., Crosthwait, R. W., and Jordan, G. L.: Necrotizing fasciitis. J. Trauma, 4:149, 1964. 5. Fallon, J.: Hemolytic streptococcal subcutaneous gangrene. Arch. Surg., 19:1817, 1929. 6. Goodall, P.: Progressive postoperative subcutaneous gangrene following excision of carcinoma of the rectum. Brit. J. Surg., 50:983,1963. 7. Grant, M. D., Horowitz, H. I., and Lorian, v.: Gangrenous ulcer and septicemia due to citrobacter. New Eng. J. Med., 280:1286,1969. 8. McCafferty, E. L., Jr., and Lyons, C.: Suppurative fasciitis as an essential feature of hemolytic streptococcal gangrene. Surgery, 24:438, 1948. 9. Meade, J. W., and Mueller, B.: Necrotizing infections of subcutaneous tissue and fascia. Ann. Surg., 168:274-280, 1968. 10. Meleney, F. L.: Hemolytic streptococcus gangrene. Arch. Surg., 9:317, 1924. 11. Meleney, F. L.: Hemolytic streptococcus gangrene: importance of early diagnosis and early operation. J.A.M.A., 92:2009, 1929. 12. Meleney, F. L.: Bacterial synergist in disease processes, with confirmation of synergistic bacterial etiology of certain types of progressive gangrene of the abdominal wall. Ann. Surg., 94:961, 1931. 13. Meleney, F. L.: A differential diagnosis between certain types of infectious gangrene of the skin with particular reference to hemolytic streptococcus gangrene and bacterial synergistic gangrene. Surg. Gynec. Obstet., 56:847,1933. 14. Rea, W. J., and Wyrick, W. J., Jr.: Necrotizing fasciitis. Ann. Surg., 172:957, 1970. 15. Saksena, D. S., Block, M. A., McHenry, M. C., et al.: Bacteroidaceae: anaerobic organisms encountered in surgical infections. Surgery, 63:261, 1968.

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16. Shires, G. T.: Care of the Trauma Patient. New York, McGraw-Hill Book Co., 1966, pp. 137-151. 17. Stone, H. H., and Martin, J. D., Jr.: Synergistic necrotizing cellulitis. Ann. Surg., 175: 702,1972. 18. Strasberg, S. M., and Silver, M. S.: Hemolytic streptococcus gangrene. An uncommon but frequent fatal infection in the antibiotic era. Amer. J. Surg., 115:763,1968. 19. Tondra, J. M.: Gangrene of the skin due to allergic reaction. Plast. Reconstr. Surg., 43: 392,1969. 20. Webb, H. E., Hoover, N. W., Nichols, D. R., et a!.: Streptococcal gangrene. Arch. Surg., 85:969,1962. 21. White, W. L.: Hemolytic streptococcus gangrene: report of 7 cases. Plast. Reconstr. Surg., 11 :1,1953. 22. Wilson, B.: Necrotizing fasciitis. Amer. Surg., 18:416,1952.

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