Acta chir belg, 2007, 107, 29-36

Necrotizing Fasciitis : Case Report and Review of Literature

L. Smeets, A. Bous, O. Heymans Department of plastic and reconstructive surgery, CHU Liege.

Key word. Necrotizing fasciitis. Abstract. We report a case of necrotizing fasciitis of the lower limb. This medico-surgical emergency is a life-threatening invasive soft-tissue infection which primarily involves the fascia superficialis and rapidly extends along subcutaneous tissue with relative sparing of skin and underlying muscles. Clinical presentation includes fever, signs of systemic toxicity and pain out of proportion to clinical findings. Paucity of cutaneous findings early in the course of the disease makes diagnosis challenging. The confirmation of the diagnosis is often made after surgical debridement. Delay in diagnosis and/or treatment correlates with poor outcome, leading to sepsis and/or multiple organ failure. Radiologic studies including plain radiographs, CT-scan or MRI may help to diagnose necrotizing fasciitis. Prompt surgical debridement, intravenous antibiotics , fluids and electrolytes management and analgesia are mainstays of the therapy. Adjuvant treatments like clindamycin, hyperbaric oxygen therapy and intravenous immunoglobulins are discussed.

Introduction Necrotizing soft-tissue infections are actually a disease with a severe outcome characterised by a fulgurous progression of the inflammation in soft-tissue with a disastrous immediate prognosis and risk of major functional sequellae. Only prompt diagnosis and rapid care, including an immediate use of appropriate antibiotherapy and extensive surgical treatment, can improve the outcome. We report a case of limb necrotizing fasciitis. We review diagnosis and treatment to allow fast recognition and adequate management of this disease entity.

Case Report

An 49-year-old woman, with chronic Leriche syndrome (aorto-iliacal arterial thrombosis) and history of drug abuse (ethylism and heroin addiction), reported acute right crural pain, increasing at walk. At first examination, clinical findings only included high fever, intensive pain and a right heel phlyctena. At the third day, puncture for right knee swelling and a suspected septic arthritis remained negative. High inflammation was evidenced in routine serology. Differential diagnosis were thrombophlebitis and osteomyelitis, but doppler and scintigraphy remained negative. On the following day, there was a great increase of the pain and a swelling of the medial part of the thigh at physical examination. Pelvic CT-scan and angioscan showed a hypodensity of

the vastus medialis without significant vascular lesions. On the next day, infectious myositis was suspected and the patient received 6 gr/day of Amoxicilline-clavulinate. Despite the antiobiotherapy, swelling and pain further increased. A cutaneous necrosis appeared and RMI demonstrated an extensive muscular necrosis of the thigh with a posteromedial collection. The patient was immediately transferred to the university hospital. At admission, very important swelling, necrotic phylctena and slight hypoesthesia of the thigh were found at examination. The patient was extremely algic and anxious with severe tachycardia and very high CRP (357 mg/ml) and CPK level (1698 U/l). Just after initial evaluation, the area of cutaneous necrosis extented from 10 cm2 to 400 cm2 in three hours (Fig. 1).The patient underwent prompt surgery consisting in wide fasciotomy and debridement of extensive necrosis of subcutaneous fat and vastus lateralis (Fig. 2). Anatomopathogy revealed a necrotizing fasciitis and an ischaemic muscular necrosis. Microbiology revealed group A streptococcus and staphylococcus. Clindamycin and Penicillin were introduced as new antibiotherapy. Despite of daily debridements of necrotic tissues and intensive supportive care, evolution was complicated by severe acute respiratory syndrome with septic shock treated by vasoactive amines. The patient was maintained under respiratory assistance during eight days. She stayed 17 days in the intensive care unit. She was transferred to the department of plastic surgery for local wound care (Fig. 3). Axillo-femoral by pass was later perfomed to alleviate chronic ischaemia of the lower limbs. The extensive tissue loss finally resulted in a high tigh amputation.

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Fig. 1 Cutaneous necrosis just after initial evaluation in the university hospital.

Fig. 3 Daily wound care in the plastic surgery departement

Fig. 2 Extensive necrosis of subcutaneous fat and vastus lateralis

Discussion Anatomopathology The course and evolution of the necrotizing fasciitis (NF) observed in our case is very pathognomic. It is an instructive illustration of a rare disease entity. We discuss some aspects of NF, in the light of our observation. Besides superficial skin infections such as erysipelas and dermohypodermal infections (unfortunately named cellulitis), there are necrotizing soft-tissue infections also called necrotizing fasciitis. They are characterized by a soft-tissue involment extending down to the fascia superficialis (Fig. 4). The most difficult step is the recognition of the deep soft-tissue infection leading to an accurate treatment decision.

The common fact between these different presentations is a necrosis involving the fascia superificialis and subcutaneous tissue, containing vessels and nerves. Inflammation induces venous micro-thrombosis, arterial vascularitis, local haemorrhage and secondary skin infarctions. Edema rapidly extends as a consequence of the release of bacterial toxins. When liquefactive necrosis of the superficial fascia and fat takes place, it produces a watery, thin, and often foul-smelling fluid known as dishwater pus. Dermal and hypodermal tissue are severely infiltrated by inflammatory cells (mainly neutrophils) (1). Epidermal and muscular structures are typically not involved. However, infection can spread to underlying muscles, resulting in myonecrosis. Haemorrhagic bullaes can develop as infection progresses (2). In presence of Clostridium species, gas production can be observed. Rapid extension of the lesions is complicated by systemic disorders. As organisms and toxins disseminate into the bloodstream, the patients develop signs and symptoms of sepsis. Hypocalcemia can develop as a result of extensive fat necrosis (3). Mortality attains 30% with higher mortality in the elderly (4). Some authors report a mortality rate as high as 76% (5). Microbiology and pathogenesis NF consists in bacterial invasive infection. The clinical presentation (including systemic disorders) changes in function of the bacteria species involved. Guilianio suggested a classification for NF based on the wound microbiology (6). Bruin-Dubuisson has adapted this classification to allow a correlation of the clinical features with the bacterial etiology (Table I) (7). There are two main categories of NF with different outcome and therapeutic strategy.

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Fig. 4 Anatomy and infections of the skin Table I Classification , clinical aspects, anatomopathology and microbiology of Necrotizing Fasciits, Adapted from : (7)
Type Pain Cutaneous signs Systemic signs Progression Type 1 + / ++ Edema, erythema, bullae, necrotic and ulcerated lesions + to +++ Moderate (3 to 14 days) Type 2 ++ / +++ Edema, erythema, necrotic bullae + to +++ (Toxic shock) very fast (Toxic shock syndrom, 1-3 days) + to +++ -/+ (secondary) Trauma, surgery, cutaneous lesion, burn, erysipelas, varicella Vascular disease Group A Streptococcus Clostidium fascitiis + Minor : oedema, pale skin + Moderate (> 3 days) Clostridium Myonecrosis +++ Pale skin, Necrotico-hemorragic bullae, anesthesia +++ Very Fast (1-3 days)

Gas production Deep fasciasinfection Muscular infection Site of entry, initiating factor Risk factors Miocrobiology

+/- to ++ -/+ (secondary) Wound, vascular lesion, surgery, local infection Diabetes mellitus Enterobacteraci ae, Anaerobes, Streptococcus, Staphyloccocus

++ Wound, surgery Diabetes mellitus C. perfingens

+++ +++ +++ Non penetrating trauma, limb crushing, IM injection, sepsis Immunosuppression C. perfingens C. septicum

Type 1 Type 1, which represents approximately 80 to 90% of all NF cases, includes polymicrobial infection involving non- group A streptococci plus anaerobes and/or facultive anaerobes (4). Perineal and abdominal (particulary postoperative) fasciitis usually belong to type 1. Four to five different bacterial species are usually found in the same lesion but some series reported as many as 11 different organisms (6). Table II lists organisms most fre-

quently implicated in necrotizing fasciitis. Enterococci and gram aerobic/anaerobic enteric bacilli are the most commonly involved species. A particular type of necrotizing fasciitis is caused by the marine vibrios. The usual site of entry is a puncture wound by a fish, a cut or an insect bite exposed to sea water (8, 9). Another special category must be made for type 1 NF that develops spontaneously, without trauma or pre-

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Table II Microbiology of Necrotizing fascitiis
Gram-positives Group A streptococcus Group AB streptococcus Enterococcus spp Coagulase-negative staphylococci Staphylococcus aureus Bacillus spp Corynebacterium spp Escherishia coli Pseudomonas aeruginosa Enterobacter cloacae Klebsiella spp Proteus spp Serratia spp Acinetobacter calcoaceticus Citrobacter freundi Pasteurella multicoda Bacteroides spp Clostridium spp Peptostreptococcus spp Prevotella spp Fusobacterium spp Veilonella spp Lactobacillus spp Propionibacterium spp Vibrio vulnificus Vibrio parahemolyticus Vibrio Damsela Vibrio algynolyticus Candida spp Aspergillus spp Rhizopus

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streptococcal toxic shock syndrome (SST) characterised by hypotension and multiorgan failure. Streptoccocus seems to be responsible for fulminating presentations. Pathogenesis of these infections has been well studied and virulent factors identified. These include factors that mediate attachment to host cells like protein F, lipotechoic acid and M protein. Group A Streptococcus (GAS) also produces a number of extracellular exotoxins that contribute to virulence, including streptokinase, streptolysin O and S, hyalouronidase, DNAses A, B, C and D. In addition, certain types of GAS produce streptococcal pyrogenic exotoxin B. This toxin is responsible for the fever and play an important role in septic shock genesis by stimulating the production of TNF, Interleukin 1 and 6 by mononuclear cells. Toxins are not the only factors implicated in the pathogenesis of streptococcal septic shock, because Streptococcus also expresses an important number of superantigens. Superantigens are molecules that bind simultaneously to a class 2 MHC molecules and to the receptor of T lymphocytes. This liaison activates a polyclonal population of T helper lymphocytes, producing an enormous amount of cytokins that mediates systemic toxicity. As in staphylococcal toxic shock syndrome, streptococcal SST appears to be a superantigen mediated process (in contrast with staphyloccocus, it has been difficult to assign an essential role to any single antigen in the pathogenesis of the streptococcal SST). Etiology and risk factors

Gram-negatives

Anaerobes

Marine Vibrios

Fungi

existing lesions. It occurs in patients with immunodefiency or neutropenia. The diagnosis is sometimes difficult because of minor cutaneous lesions, whereas pain and systemic toxicity signs are often important. Enterobacteraciae (E. coli), clostridium spp and Pseudomonas are usually present. A separate class of NF is reserved for clostridium gas gangrene with or without myonecrosis. It is charecterised by the production of gas in fascias and muscles. The superficial type is associated with a blunt trauma or a surgical intervention. The deeper type with myonecrosis, is found after non-penetrating trauma with crushing or intramuscular injection. As type 1-like NF, it sometimes occurs spontaneously by hematogenous spread of clotridium bacteria, typically in patients with digestif neoplasia (usually C. Septicum is involved) (10). Type 2 Type 2 necrotizing fasciitis is a monomicrobial infection by Group A streptococcus. Necrotizing fasciitis of the extremities and limbs is usually type 2 (11). These lesions can be complicated by septic shock known as

Necrotizing fasciitis is caused by the spread of pathogens in the subcutaneous tissue. Reported etiologies of soft-tissue injury leading to necrotizing fascitiis include blunt or penetrating trauma, direct inoculation of the subcutaneous tissue from a superficial site and hematogenous spread from a distant site. Occuring in any region of the body, NF most commonly involves the abdominal wall, extremities and perineum (Fournier gangrene). Table III lists the most common localisations and etiologies of necrotizing fasciitis. Fasciitis of the face and neck is type 1 or 2 in adults, usually following ORL or dental infection (Haemophilus influenza is also found in children). In this location, the infection easily spreads via fascial planes into deep cervical spaces or vascular compartments. Many complications of cervical fasciitis have been described, including airway obstruction, jugular venous thrombosis, mediastinitis, rupture of great vessels, empyema and lung abscess (12-14). With a susceptibility to cutaneous infections, diabetics are at high risk to develop NF. In the lower limbs, development of NF is enhanced by vascular and lymphatic

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Table III Etiologic aspects of necrotizing fasciitis
Limbs and extremities Trauma (blunt or penetrating) Bite (animal or insects) Drugs Subcutaneous injection (insuline e.g) Cutaneous infection (folliculitiis, abcess or ulcers e.g) Appendicitis Colocutaneous fistula Perforated viscus Diverticulitis Renal calculus Bartholinitis Vulvar abscess Hysterectomy Episiotomy Caesarean Salpingectomy Coital injury Prostatic surgery Genitourinary infection Pilonidal abscess Hemorrhoidal banding Rectal carcinoma Cervical adenitis Otologic infections Peritonsillar abscess Dental abscess Salivary gland infection

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The stereotypical course of NF involves a normal or slighty inflammed soft-tissue area that suddenly progresses to overt fasciitis, accompanied by systemic toxicity. At this state, the local signs most commonly associated with NF are (7) : a rapidly progressive oedema, overstepping widely the inflammatory area. bullae filled with serous fluid becoming hemorragic or purulent, sometimes malodorous. blue-grey cyanotic lesions (associated with thrombosis of cutaneous perforating vessels) and pale ischaemic areas. an erythema without distinct borders (in contrast to erysipelas) As infection extends, the overlying skin becomes smooth, shiny and tensely swollen. Within one or two days, lesions colour progressively changes, from red to purple to blue and then becomes frankly gangrenous by the fourth or fifth day, turning black. In clostridium infection, crepitances suggest production of gas. The infection progresses to nerve necrosis with hypoesthesic or anaesthesic skin areas. NF is rarely diagnosed before this stage. A series of 89 patients with NF reported a correct initial diagnosis of NF on first presentation in only 15% of cases, with cellulitis (59%) and abcess (18%) as the most common misdiagnosis (17). Signs and symptoms of systemic toxicity are capital to orientate to diagnosis. High fever, tachycardia (> 90/min) and tachypnea (> 20/min) are early findings. As infection progresses, severe septic syndrome develops, with arterial pressure drop (under 90 mmHg or diminution of 40 mmHg under the habitual pressure). Oliguria (< 30 ml/h) and elevation of creatinine reflect renal impairment. Pulmonary, neurologic, haematologic and hepatic complications may be associated to initial features, followed by severe septic shock with resistant systemic hypotension and hypoperfusion in absence of adequate care. Diagnosis With an high index of suspicion (crepitus at physical examination), a clinical diagnosis of NF can be made, prompting early surgical exploration to confirm diagnosis (lack of resistance to dissection of normally adherent fascia) but without soft-tissue gas. NF remains a diagnosic challenge, requiring laboratory, microbiology and radiologic investigations. Routine laboratory, including white blood cell count and C-reactive protein level, may distinguish NF from non-necrotic soft tissue infection. CPK concentration is also useful as marker of muscular necrosis. WONG et al.

Abdominal

Genital and perineal

Face and neck

stasis. Patients with peripheral vascular disease present a risk of NF development. Type 1 fasciitis commonly occurs in patients with immunosupression, as in AIDS or after corticoid therapy, or in other situations weakening host reactions to infection ( alcohol abuse, neoplasia, recent surgery, cardiac and pulmonary diseases, malnutrition, smoking,...). In children, varicella seems to be a significant factor. Concurrent use of nonsteroidal antiinflammatory (NSAIDs) drugs has been incriminated, but available prospective and retrospective studies do not support a causal relationship (15, 16). NAIDs can mask pain and symptoms of NF, and delay diagnosis. Clinical features The early diagnosis is the major challenge in NF, due to the paucity of cutaneous findings in the early course of the disease. At the beginning, patients usually present with aspecific symptoms including pain, swelling and fever. Tenderness, erythema and warm skin are commonly the only signs of NF in its early stage. Later, diagnosis of a necrotizing infection is based on the association of local and systemic signs and symptoms : an exquisite pain, completely disproportionate compaired to clinical findings, as key symptom. The intensity of local signs can be weakened by previous antibiotherapy or in immunosuppressed patients.

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have recently developed a Laboratory Risk Indicator for necrotizing fasciitis (LRINEC). A score was assigned from a combination of values for C-reactive protein, white blood cell count, hemoglobin, serum sodium and glucose (18), parameters with an early change in the infection. A low score (< 6) was associated with a less than 50% probability of having NF, and a high score (> or equal to eight) with a greater than 75% probability of NF. This model has not been prospectively analysed. Hemoculture and aspirates of cutaneous lesions or bullae with a thin needle are often sterile, due to a prior antibiotherapy. Peroperatorive culture with antibiogram leads to bacterial species identification and to adequate antibiotic treatment. Biopsy is also helpful as an alternative diagnostic method. Radiologic studies are also contributive but should never delay appropriate surgical treatment of highly suspicious cases. Radiographies are more sensitive to detect gas than physical examination (19). Unfortunately, the production of gas is highly variable and tend to appear late in the course of NF. Presence of gas excludes a type 2 fasciitis. CT scanning is more accurate in detecting gas tracking along fascial planes than plain radiographies (20). CT scan identifies subcuteaneous and fascial thickening, foreign bodies and focal fluid collection (abscess). It also delineates the spread of infection, especially in cervical fasciitis. However, oedema of soft-tissue can lead to overestimation of lesions. Finally, CT scan sometimes does not adequately differentiate between severe cellulitis and NF, and cases of NF with negative CT findings have been reported (21). Magnetic resonance imaging has the highest sensitivity (93-100%) for diagnosing NF. NF exhibits high signal intensity on T2-weighted images by MRI with hyperintense signal corresponding to fluids associated with NF. Using MRI, RAHMOUNI et al. were able to separate necrotizing soft-tissue infections which warrant immediate surgical intervention from non-necrotizing cellulitis, which can be treated medically (22). However, hyperintense signal can be seen in other diseases with fascial edema without necrosis as cellulitis, abscess, lymphatic obstruction, rheumatic disease, recent surgery or passive oedema (congestive heart failure, cirrhosis). In Fournier gangrene, scrotum ultrasonography has been used to reveal skin thickening and swelling, with subcutaneous, hyperechoic foci representating gas (23). The role of ultrasonography in the evaluation of NF in other areas of the body is less evident. Treatment Treatment modalities include aggressive surgical debridment, broad-spectrum antibiotics, haemodynamic support and general cardiorespiratory supportive care to

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maintain vital organ functions. Hyperbaric oxygen and immunoglobulins do not have firm evidence supporting their use. WONG et al. (17) analysed factors correlated to adverse outcome. Three factors were found to affect survival : advanced age, presence or two or more associated comorbidities, and delay from admission to operation of more than 24 h. Surgery The first choice treatment of NF remains surgery including early debridment of all necrotic tissues and drainage of involved fascia planes via extensive fasciotomy. Prompt surgery has been associated with improved survival, compared to delayed intervention (5, 24). Surgery should be performed within 24 h of presentation as the mortality rate significantly increases beyond this period (17). Wide resection of all devitalized tissues is the key of adequate surgery. Limited resection or drainage are inappropriate. Re-exploration and further debridements are often required to achieve control of the necrotizing process. Repetitive interventions are the rule and survival has been documented after excision of as much as 45% of a patients surface area (25). Surgical wounds must be frequently reevaluated for evidence of disease extension. In perineal NF, diverting colostomy and/or urinary diversion are often needed to control infection. Amputation of extremities is sometimes necessary, particularly in patients with diabetes and/or peripheral vascular disease. Reconstructive procedures, including skin grafting, flap or free flap are often required. Antibiotics Parenteral antimicrobial therapy must assure broad coverage for a wide range of pathogens including aerobic gram-positive, gram-negative organisms and anaerobes. However, there are no guidelines for specific initial antibiotic therapy. Despite appropriate and early antibiotic use, infection may progress because of thrombosis of superficial vessels precluding effective antibiotic penetration. In this case, the main goal of antibiotherapy is infection control, avoiding hematogenous dissemination, while waiting surgical intervention. A beta-lactam/beta-lactamase combinaison such as ampicillin/sulbactam, piperacillin/tazobactam or ticarcillin/clavulinate are reasonable empiric choices despite increasing resistance of enteric pathogens. For penicillinallergic patients, clindamycin and aztreonam association is an acceptable alternative. Third or fourth-generation cephalosporins with metronidazole or clindamycin for anaerobe coverage are also recommended. Antimicrobial therapy should be tailored to culture and susceptibility results. Extended coverage with vancomycin has to be added for nosocomial infections (Pseudomonas spp, highly resistant gram-postive bacteria) or surgical wound contamination.

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For type 2 fasciitis, high-dose penicillin remains the best option. Animal and human studies suggest beneficial effects of adding clindamycin in type 2 NF because clindamycin may suppress production of exotoxins and/or virulence factors and enhance phagocytosis by inhibiting M-protein synthesis (26). Retrospective data suggest a benefit of clindamycin in invasive group A streptococci disease. In Clostridium fasciitis, penicillin/clindamycin is also the treatment of choice. Supportive care After initial debridement, the cooperation of intensivists, surgeons and infectious disease specialists is crucial for optimal care. Patients require early intensive care for metabolic and haemodynamic support. Adequate nutritional support improves survival (4, 27). As in burn victims, patients may loss fluids, proteins and electrolytes from a large surgical wound. Fluid and electrolyte resuscitation and analgesia are the mainstays of support for patients with advanced sepsis usually combined with vasoactive amines associated with mechanic ventilation. With persistant inflammation and intravascular coagulation, patients are at high risk of thrombosis. As thrombo-embolic complications are the second cause of mortality (7), appropriate anticoagulation therapy is needed. Equilibration of diabetes, correction of metabolic acidosis and renal failure are also an important part of management. Adjuvant therapy Use of hyperbaric oxygen (HBO) is based on animal studies, case reports, and retrospective studies (28). The physiologic effects of HBO have been shown to include increased killing ability of leukocytes, reduction of oedema, promotion of angiogenesis and wound healing. Direct effects on anaerobes are caused by elevation of oxydoreduction potential producing NADPH and NADH consumption, and production of free radicals enhancing bacterial death. Retrospective analyses suggest benefits both in mortality and in morbidity for HBO in the setting of NF but these results have not been prospectively validated. However, HBO use in anaerobic infection such as clostridial gangrene is supported by experimental data and should be instituted before surgical intervention (29). In NF, if HBO therapy is available, it should be considered as additional treatment but should never preclude nor postpone early surgical debridement. Free radical production is a physiologic complication of HBO with pulmonary oxygen toxicity (edema and sometimes evolution to fibrosis) and reversible myopia (up to 20%). Barotrauma complications (pneumothorax, otobarotrauma, tympanic rupture, etc) are exceptional. Perfusion of immunoglobulins is another adjunctive treatment in streptococcal NF which could reduce

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mortality (30-33). Several mechanisms of actions are proposed, including direct opsonization, antagonization of bacterial superantigens and modulation of immune cytokine responses through unidentified pathways. This treatment remains expensive and without consensus on the optimal dose. Risks associated to their use are renal failure and anaphylaxis (in patients with IgA deficiency). Conclusion Despite antibiotic therapy and surgical intervention, the mortality and morbidity of NF remain high. Only early identification of the necrotizing process can improve the outcome of this life-threatening disease. NF should be suspected in every skin infection with fever, signs of systemic toxicity and severe pain. An adequate use of radiologic procedures should not delay surgical debridement. Future diagnostic clues, including transcutaneous oxymetry, might advance our ability to provide prompt therapy. New potential treatments for group A streptococci NF could be vaccines, new antibiotics and superantigen directed therapies such as neutralization and inhibition of production of super-antigens by streptococci.

References
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L. Smeets Department of Plastic and Reconstructive Surgery CHU Lige