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Original Research

Large Flap Preservation in a Patient With Extensive Necrotizing Fasciitis

June 2010
WOUNDS. 2010;22(6):146-150.

Abstract

Necrotizing fasciitis is a rare yet rapidly progressive life-threatening soft tissue infection. Historically, radical excision (including skin) along with broad-spectrum antibiotics has been the treatment regimen of choice. The authors report a patient treated in the burn unit with extensive necrotizing fasciitis in whom large skin flap preservation was achieved. The staple treatment of necrotizing fasciitis is early recognition, diagnosis, and complete necrosectomy. This process often leads to unnecessary resection of all overlying skin beyond the sentinel region of infection. To the authors’ knowledge, the preservation of large skin flaps in patients with necrotizing fasciitis has not been reported in the literature.

Introduction

Necrotizing fasciitis is a soft tissue infection that travels along a plane between the fascia and deep subcutaneous tissues. Aggressive and radical excision of all purulent and necrotic tissue must be completely excised without reservation eliminating further migratory spread of infection. In the past, total radical excisions may have included complete removal of all overlying skin.1 More recent studies have classified the degrees of skin viability,2 which are very similar to assessing burn injury zones of coagulation, stasis, and hyperemia. These observations take a closer look at the pathophysiological signs of skin flap viability. This may serve as a viable adjunct to efficiently optimizing perioperative wound management. The following report illustrates the clinical outcome of a patient who underwent radical excision of necrosis while achieving skin flap preservation. The purpose of this report is to describe our burn center’s surgical approach to performing a complete necrosectomy with large skin flap tissue preservation in a patient with necrotizing fasciitis.
 

Case Report

A 55-year-old white man with no significant past medical history initially presented to an outside hospital (OSH) with a 3-week history of general malaise with subsequent development of a perirectal boil. The CT scan and the OSH demonstrated an abscess in the bilateral buttock with subcutaneous extension into the right iliac crest, flank, and scapula regions. The diagnosis was necrotizing fasciitis. The OSH admission vitals were: temperature 100.5˚F, pulse rate 118, blood pressure 117/68, and respiratory rate 20. His initial labs at the OSH included a 10.5 WBC, 67 Segs, 24 Bands, 7000 CK, and 10.2 hemoglobin. The patient underwent two surgical debridements, developed septic shock and respiratory failure, and was placed on vancomycin, metronidazole (Flagyl), tigecycline, and ceftriaxone at the OSH before he was transferred to the authors’ burn center. His initial cultures at the OSH grew beta-hemolytic streptococcus, bacteroides fragilis, and peptostreptococcus with gram-positive cocci bacteremia. The patient arrived at the authors’ burn center vented and on levophed with pulse rate of 78 and blood pressure of 103/55. The patient was also diagnosed with new onset Type II diabetes. The infection involved a total body surface area (TBSA) of 17% including areas overlying the buttocks, back, right flank, and right abdomen (Figure 1). The patient was taken to the operating room immediately upon arrival. There was persistent centrifugal spread of infection along the fascia. Streptococcus anginosus, a Group C streptococcal species, was found to be the causative organism. The sepsis resolved on postoperative day (POD) 1. The patient was extubated on POD 2. His initial antibiotic regimen from the OSH was discontinued and he received 11 additional days of IV Primaxin at our facility.

Surgical technique and decision-making. The patient was taken to the operating room for surgical exploration and complete necrosectomy. Full-thickness incisions were made at the right anterior abdominal wall, axilla, buttock, and sacral regions to visually track and halt the centrifugal spread of infection (Figure 2). The leading edge of purulence and infection migrating along the fascia was identified and excised via radical necrosectomy. Healthy fascia was left intact while angiothrombosis and dermal hemorrhage in the skin and soft tissue were used as indicators of extensive vertical transmission of infection. Patent microvasculature in the soft tissue above the fascial planes was used as a sign of potential viability (Figure 3). Serial, meticulous debridement of the wound and skin flaps (every 1–2 days for a 5-day period) was performed after the initial radical necrosectomy. Integra (Integra Life Sciences, Plainsboro, NJ) was placed over a healthy bed of granulation tissue to cover the remaining defect.

Perioperative wound care and closure. Initially, the dressings involved gauze negative pressure wound therapy (NPWT) with topical sulfamylon irrigations. Once the wound bed and skin flaps were clean negative pressure wound therapy ([V.A.C.® Therapy], Kinetic Concepts Inc, San Antonio, TX) was placed over the right axilla, anterior torso, posterior torso, buttock, and right flank wound beds. The skin flaps were approximated with interrupted nylon suture and positioned over the NPWT foam. NPWT dressing changes were performed every 4 days (Figure 4). The defect was serially closed with interrupted Vicryl by suturing the granulated skin flaps to a healthy granulated wound bed. Advances in wound care, such as NPWT, have proven to be very useful adjuncts in postoperative wound management.3,4

Results

After 2 months of meticulous wound care, preservation of large skin flaps, and reconstructive surgery, the patient had an unremarkable recovery. The initial wound comprised 17% TBSA (3553 cm2) of which 47% was preserved skin flaps. Integra placement followed by split-thickness skin grafting and a V-Y advancement flap were used to cover the remaining 41% (1463 cm2) of the torso and 5.8% of the sacral region, respectively. The wound was completely closed at discharge; however, clinic follow-up has been uneventful and involved observation for scar development.

Discussion

Hippocrates first described necrotizing fasciitis in the fifth century BC. Necrotizing fasciitis is a fulminating and morbid form of necrotizing soft tissue infection.5 Necrotizing fasciitis is a formidable disease that initially requires a high degree of suspicion followed by early diagnosis, prompt surgical exploration, and targeted antibiotic therapy. The offending microorganisms are categorized into a type I (monomicrobial staphylococcus, streptococcus, klebsiella, E coli, and anaerobes) and the more common type II polymicrobial infection.6 Mortality rates in the literature vary up to 73%2 and may stem from multiple comorbidities, but unequivocally are due to delayed diagnosis and surgical treatment.7–19 Various studies serve as diagnostic adjuncts.15 However, a definitive diagnosis is made during the initial surgical wound exploration. Patients with extensive disease(s) are often left with large, morbid wounds that are difficult to manage perioperatively (Figure 1). More recently, a shift has occurred in referral to burn centers for large wounds and skin loss conditions. Burn centers possess the multidisciplinary team expertise to cost effectively provide the critical care, wound closure, and reconstructive and rehabilitative needs of these patients.20 The ultimate surgical goal is to perform a complete necrosectomy with immediate eradication and cessation of infection during initial exploration.11 Consideration should be given to the fact that the centrifugal spread of necrotizing fasciitis is not always directly proportional to its vertical transmission of disease. This may alleviate the need for the skin excision to be as wide as the fascial debridement. Skin that is obviously necrotic should be excised without hesitation. However, the cellulitic skin and soft tissue not overlying the sentinel region of infection should be closely evaluated for the clinical and pathophysiological signs of devitalization secondary to extensive vertical transmission of disease. Skin and soft tissue without thrombosed microvasculature may possess direct and collateral circulation that will promote and generate healthy granulation tissues. Meticulous and serial surgical debridement coupled with NPWT dressings may contribute to fostering the development of healthy skin flap granulation suitable for closure, thereby affording flap preservation as a potential and viable adjunct to perioperative wound management in patients with necrotizing fasciitis.

Conclusion

Surgical necrosectomy that is swift, complete, and without compromise should remain as the standard of care for necrotizing fasciitis. However, a surgical mentality of “everything including the kitchen sink” is not always indicated. The change in this thought process may afford the opportunity to better understand and differentiate between the centrifugal spread and vertical transmission of this disorder, thereby improving clinical assessment of pathophysiological signs of skin and soft tissue non-viability that is imperative to optimizing perioperative wound management and closure. Larger studies are necessary in order to warrant routine large skin flap preservation.

Acknowledgements

From the Department of Surgery, Wright State University, Boonshoft School of Medicine. Address correspondence to: Travis L. Perry, MD Wright State University, Boonshoft School of Medicine Department of Surgery One Wyoming St., 7800 WCHE Dayton, OH 45409 Phone: 937-208-2177 Email: Travis.perry@wright.edu.

References

1. Bilton BD, Zibari GB, McMillan RW, Aultman DF, Dunn G, McDonald JC. Aggressive surgical management of necrotizing fasciitis serves to decrease mortality: a retrospective study. Am Surg. 1998;64(5):397–401. 2. Wong CH, Yam AK, Tan AB, Song C. Approach to debridement in necrotizing fasciitis. Am J Surg. 2008;196(3):e19–24. 3. Elliott DC, Kufera JA, Myers RA. Necrotizing soft tissue infections. Risk factors for mortality and strategies for management. Ann Surg. 1996;224(5):672–683. 4. Kotrappa KS, Bansal RS, Amin NM. Necrotizing fasciitis. Am Fam Physician. 1996;53(5):1691–1697. 5. Descamps V, Aitken J, Lee MG. Hippocrates on necrotizing fasciitis. Lancet. 1994;20;344(8921):556. 6. Sarani B, Strong M, Pascual J, Schwab CW. Necrotizing fasciitis: current concepts and review of the literature. J Am Coll Surg. 2009;208(2):279–288. 7. Kaiser RE, Cerra FB. Progressive necrotizing surgical infections – a unified approach. J Trauma.1981;21(5):349–355. 8. Nichols RL, Smith JW. Gas in the wound: what does it mean? Surg Clin North Am.1975;55(6):1289–1296. 9. McHenry CR, Piotrowski JJ, Petrinic D, et al. Determinants of mortality for necrotizing soft-tissue infections. Ann Surg. 1995;221(5):558–563. 10. Wong CH, Chang HC, Pasupathy S, Khin LW, Tan JL, Low CO. Necrotizing fasciitis: clinical presentation, microbiology, and determinants of mortality. J Bone Joint Surg Am. 2003;85-A(8):1454–1460. 11. Voros D, Pissiotis C, Georgantas D, Katsaragakis S, Antoniou S, Papadimitriou J. Role of early and extensive surgery in the treatment of severe necrotizing soft tissue infections. Br J Surg. 1993;80(9):1190–1191. 12. Rea WJ, Wyrick WJ Jr. Necrotizing fasciitis. Ann Surg. 1970;172(6):957–964. 13. Majeski JA, Alexander JW. Early diagnosis, nutritional support, and immediate extensive debridement improve survival in necrotizing fasciitis. Am J Surg. 1983;145(6):784–787. 14. Elliott D, Kufera JA, Myers RA. The microbiology of necrotizing soft tissue infections. Am J Surg. 2000;179(5):361–366. 15. Saiag P, Le Breton C, Pavlovic M, Fouchard N, Delzant G, Bigot JM. Magnetic resonance imaging in adults presenting with severe acute infectious cellulitis. Arch Dermatol. 1994;130(9):1150–1158. 16. Nowak R. Flesh-eating bacteria: not new, but still worrisome. Science.1994;264(5166):1665. 17. McGee T, Munster A. Toxic epidermal necrolysis syndrome: mortality rate reduced with early referral to regional burn center. Plast Reconstr Surg. 1998;102(4):1018–1022. 18. Warden GD, Brinkerhoff C, Castellani D, Rieg, LS. Multidisciplinary team approach to the pediatric burn patient. QRB Qual Rev Bull. 1988;14(7):219–226. 19. Kovacs LH, Kloeppel M, Papadopulos NA, Reeker W, Biemer E. Necrotizing fasciitis. Ann Plast Surg. 2001;47(6):680–682. 20. Faucher LD, Morris SE, Edelman LS, Saffle JR. Burn center management of necrotizing soft-tissue surgical infections in unburned patients. Am J Surg. 2001;182(6):563–569.

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