Necrotizing Soft-Tissue Infections: An Orthopaedic Emergency

Adam Lee, MD; Addison May, MD, FACS, FCCM; William T. Obremskey, MD, MPH


J Am Acad Orthop Surg. 2019;27(5):e199-e206. 

In This Article


Management of NSTIs is best carried out by a multidisciplinary team with experience treating large soft-tissue wounds. However, initial management should be done by the first surgeon who recognizes and diagnoses this potentially lethal infection. The mainstay of management is expeditious, soft-tissue decompression and débridement of the necrotic tissue with first broad-spectrum antibiotic management and then focused systemic antibiotic management.[31] Repeat débridements are done to ensure disease progression has halted and to remove unviable tissue. As many patients present with a systemic response or progress to systemic toxicity, intensive care unit admission with critical-care team resuscitative support is mandatory. Adjunctive management may be considered in special cases.

Surgical Débridement

When NSTI is diagnosed or is suspected based on the progression of symptoms in spite of antibiotic management, surgical intervention should take precedence. Surgery should not be delayed for imaging assessment, and resuscitation and antibiotic administration should be ongoing concomitantly in preparation for surgery.[32] Broad decompression and débridement of the infected tissue helps to halt progression and allows for antibiotics to take effect and for the host's immune system to respond.[3] Débridement should begin with a longitudinal incision over the nidus of infection (ie, entry site, site of abscess, site of original erythema/necrosis). In the early phase, a simple skin and subcutaneous incision down to fascia and extended proximally until uninvolved tissue is encountered is required. If the underlying muscle is involved or notable muscle swelling is present, the underlying fascia should be incised as in a compartment release. Often, dual incisions are required on the extremities to ensure adequate decompression is attained as in compartment syndrome. Devitalized tissue should be removed in all affected layers (eg, skin, subcutaneous fat, fascia, muscle, bone) until healthy tissue margins are reached (Figure 3, A and B). Multiple deep tissue cultures should be collected for microbiologic analysis. Débridement should proceed with no regard for late reconstruction because this may bias a surgeon to leave disease-burdened tissue. Amputation is required if the progression of the infection is so rapid that débridement alone would not be adequate, the limb is not salvageable because of notable tissue loss or if the condition of the patient does not allow repetitive débridements. Guillotine amputations above the level of progression are the most direct form of amputation and should be considered at the extreme end of the surgical algorithm. In less progressive cases, small ladder incisions may be used to assess more proximal sites of progression. If diagnosis is equivocal, a smaller incision can be made to assess for deep fluid or tissue plane disruption (finger test). Once a thorough débridement is complete, wounds are dressed according to their location and practical application. Moist gauze packing is the simplest dressing and may be useful early when frequent débridements are ongoing. Vacuum-assisted closure can be used and aids in preparing wounds for subsequent closure, graft, or flap.[33] Early surgical débridement is so important to limb salvage and patient survival in which initial débridement should be considered before transferring a patient to a higher level of care for intensive care and reconstruction. The initial débridement is not complicated or technically difficult and should be treated similarly to compartment syndrome where initial surgical débridement can be done by any surgeon and then transfer the patient if needed for extended care.

Figure 3.

Photograph showing (A and B) extensive dual incision fasciotomy with negative pressure wound therapy placement. Immediately after fasciotomy, notable decrease in erythema is seen.

The reason for the success of a simple incision over the area involved is not completely clear. Surgical incision and débridement decreases the source and bacterial load, but the condition of the skin and subcutaneous tissue improves quickly after the skin incision is extended proximally into healthy tissue. The decompression seems to halt the bacteria that spread in the fascial layers and lymphatic system. The incision may allow decompression and abort the cycle of local tissue inflammation and edema that drive the proximal spread of the disease process.

Early surgical re-exploration is recommended within 24 hours of initial débridement and has been shown to decrease mortality and rate of acute kidney injury compared with repeat débridements done at greater than 48 hours.[17] The same principles apply to subsequent débridements as to the initial débridement. The average number of surgical procedures in the management of NSTI in large series ranges from 2 to 5 times.[10,26,28,34,35]

When the clinical course has improved and no signs of progression of disease have manifested for several days, reconstruction procedures can be pursued. The sooner the decompression is done, the less the necrotic tissue needs to be removed and allows wounds to undergo primary closure or skin grafting although occasional local or free soft-tissue transfers are necessary, and nearly half of all patients will need some form of coverage.[32–34] One large retrospective study reported an average of 1.2 reconstructive procedures in each case of NSTI.[26]


Antibiotic administration complements the surgical débridement as a means to further decrease infective load. Broad-spectrum empiric antibiotics should be administered on presentation based on the presenting history, patient risk factors, and possible exposures. Most hospitals will have an infectious disease protocol for empiric antibiotic treatment in the critically ill based on local virulence patterns and antibiogram. A broad-spectrum, synergistic penicillin (ie, piperacillin/tazobactam, ampicillin/sulbactam) with clindamycin or carbapenem is included in most recommendations for empiric coverage. Because of the possibility of community acquired MRSA, vancomycin or linezolid should be added to broaden the antibiotic scope.[31,33] Blood cultures and tissue cultures further direct bacteria-specific treatment based on susceptibilities and local policies. Antiribosomal agents are recommended to (1) limit toxin production and (2) enhance the effectiveness of cell wall antimicrobial agents in setting of high bacterial burden. For gram-positive pathogens, the antiribosomal agent is most commonly clindamycin.[22] Linezolid may have similar effects on protein synthesis and has been reported as an antibiotic supplement in the management of NSTI.[36]

If gram stains of the excised tissue demonstrate the presence of gram-negative pathogens such as Tularemia, agents in the tetracycline class should be considered.

No specific, evidence-based guidelines directing antibiotic selection, mode of delivery, or duration are available. Consultation with an infectious disease specialist with experience in treating soft-tissue infections may aid in directing long-term antibiotic management.[31]


A number of adjunctive management have been attempted to supplement management of these devastating NSTIs. Given the heterogeneity of this disease process and the relatively rare occurrences, high-quality evidence of therapies used in addition to débridement and antibiotics is limited.

Adjuncts have been sought to attenuate the systemic response to disease. Intravenous immunoglobulin (IVIG) offers theoretical benefit in blunting the host's response to bacterial toxins.[20] Pooled immunoglobulins from donors previously infected with toxin-producing bacteria are thought to neutralize circulating toxins and lessen the systemic response. However, data are conflicting on the utility of this treatment with studies showing no change and notable change in outcomes.[22,37] This change may be because not all IVIG infusions contain the same proportion of antitoxin immunoglobulins. In a similar pursuit of immunomodulation, the only randomized controlled trial involving NSTIs evaluated the drug AB103, a substance that acts on T cells to decrease the immune response to toxins. Unfortunately, the authors found no changes when the novel therapeutic was compared with the placebo.[35] Corticosteroids have a similar, albeit less specific effect on the immune response to bacterial toxins have been used as an adjunct in patients with NSTI and toxic shock syndrome.[38]

Hyperbaric oxygen treatment is theorized to aid in the prevention of the progression of tissue loss and therefore morbidity and mortality. However, in a Cochrane review, no literature worth of analysis was found, and no summation of data was suggested.[39] Hyperbaric oxygen treatment may be considered if it does not interfere with access to surgical and antibiotic treatment.