Ann Thorac Surg 2001;72:1362-1364
© 2001 The Society of Thoracic Surgeons
Case report
Necrotizing fasciitis of the chest wall
David B. Safran, MDa,
William G. Sullivan, MDb
a WakeMed Hospital, Raleigh, North Carolina, USA
b University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA
Accepted for publication October 14, 2000.
Address reprint requests to Dr Safran, CARElina Surgery, Suite 304, 3024 New Bern Ave, Raleigh, NC 27612
e-mail: dsafran{at}wakemed.org
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Abstract
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Necrotizing fasciitis is a highly morbid soft tissue infection that rarely involves the upper torso. An extremely unusual case of necrotizing fasciitis of the chest wall is reported, including the method by which an open thoracic cage was managed. This represents the second reported case of a patient surviving necrotizing fasciitis of the chest wall requiring rib resection and chest wall reconstruction.
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Introduction
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It is extremely uncommon for necrotizing fasciitis to occur along the upper torso or chest wall, with only a handful of such cases having been reported. Carrying an inherently high mortality rate, between 30% and 76% [1], when occurring in other regions of the body, necrotizing fasciitis of the chest wall carries with it a particularly poor prognosis [2]. In this report, we describe the case of a patient who survived severe necrotizing fasciitis of the chest wall following thoracotomy for treatment of an empyema.
A 50-year-old man presented to the emergency department with complaints of abdominal pain, nausea and vomiting, fever, and sweats. Ensuing evaluation excluded abdominal pathology and led to a diagnosis of right lower lobe pneumonia as the etiology, as well as discovery of previously undiagnosed diabetes mellitus. The patient was started on trovafloxacin as treatment for the pneumonia. Computed tomography (CT) scan of the chest repeated 6 days later showed an extensive inflammatory, multiloculated pleural fluid collection and a small pocket of enclosed gas within one of the smaller abscess cavities (Fig 1). CT-guided thoracentesis was performed, delivering purulent fluid that grew heavy B fragilis, Prevotella spp, and Lactobacillus spp, and light E coli and peptostreptococcus. Despite appropriate antibiotic therapy, the leukocytosis persisted. Due to the multiloculated, thick-walled nature of the collection, it was felt that tube thoracostomy would be inadequate to effect adequate drainage, so thoracoscopic debridement was planned. Three days later, an attempt at thoracoscopic debridement and drainage was unsuccessful and conversion to open decortication through a posterolateral right thoracotomy was accomplished. Cultures obtained intraoperatively grew all of the above organisms, as well as nonspeciated anaerobic nonsporeforming gram-positive rods.

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Fig 1. Computed tomography scan of the chest showing extensive, multiloculated right-sided pleural collection, consistent with a diagnosis of empyema. A small gas pocket may be seen within the smaller, lateral cavity.
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The patient was extubated immediately postoperatively and transferred to the surgical intensive care unit for observation. Trovafloxacin was continued. On postoperative day 3, suppurative drainage was noted at the wound. Gram stain demonstrated many gram-positive cocci in pairs, chains and clusters, many gram-negative rods and many gram-negative cocci. Cultures ultimately grew only heavy Lactobacillus spp. and light coagulase-negative Staphylococcus aureus. That same day, the patient was returned to the operating room where the wound was formally opened and explored. Full-thickness necrosis of the chest wall was found, involving the skin, fascia, and muscle layers, including portions of the pectoralis major and minor, serratus anterior, latissmus dorsi, and the intercostal muscles. Wide debridement was undertaken, including the affected intercostal muscles and segments of the adjoining two ribs. The resultant defect in the thoracic cage was closed with polyglactin 910 mesh. Chest tubes were maintained in the pleural space and closed suction drains were placed in the recesses of the overlying soft tissue. The large wound cavity was then packed with moist gauze and left open. Tracheostomy was also performed.
Based upon intraoperative findings, antibiotics were changed to imipenem/cilastatin, penicillin G, and metronidazole. Wound packing was changed daily in the intensive care unit (Fig 2). The patient was returned to the operating room for subsequent debridements twice. On postoperative day 19, the patient was removed from the ventilator. At that time, the right lung remained expanded and could thereafter be seen to be moving freely beneath the mesh until granulation tissue had covered the entire base of the wound.

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Fig 2. Wound cavity undergoing bedside packing change. Multiple intrapleural chest tubes are seen, with closed suction Jackson-Pratt drains in the recesses of the soft tissue defect. Note the absorbable mesh covering the gap caused by rib resection.
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Following a subsequent ICU course highlighted by an episode of acalculous cholecystitis requiring percutaneous drainage, on postoperative day 53, the patient was discharged to a rehabilitative hospital, undergoing continued dressing changes for the wound. CT scan was performed on July 20, 1999, to evaluate the chest wall and pleural space (Fig 3), confirming the clinical observation of complete closure of the pleural space. Dressing changes were continued after the patient had been discharged to home and returned to work. On postoperative day 125, as an outpatient, he underwent formal delayed primary closure of a residual wound defect that measured approximately 3 inches in width and 1 inch in depth.
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Comment
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Necrotizing soft tissue infections are uncommon, seen most frequently in immunocompromised patients. These infections are often multimicrobial, although a single organism may be responsible in as many as 77% of infected patients [3]. When a single organism is responsible, Group A streptococci and Clostridium perfringens have been among the most frequently isolated pathogens [4]. Monomicrobial infections often present in a fulminate fashion, with systemic toxicity highlighted by fever, leukocytosis and, occasionally, shock. In contrast, polymicrobial infections may present in a more insidious manner. These infections are caused by synergy among anaerobes and facultative aerobes, involving both gram-negative and gram-positive organisms, and can affect any and all layers of soft tissue, including skin, fat, fascia, and muscle [4].
The infections occur most frequently along the lower aspects of the body, such as the legs, perineum, and lower abdomen. Numerous inciting incidents have been implicated, including major or minor trauma, unrecognized lower extremity ulcerations and minor infections, perirectal abscesses, and postoperative mishaps often involving violation of the gastrointestinal tract. Severe necrotizing soft tissue infections involving the upper body and chest wall, however, are distinctly uncommon. In a recent review of the literature, Urschel and others found only 9 documented cases reported through 1993 [2]. A MEDLINE search disclosed 3 more cases reported since 1993, excluding our own. Of the 12 other cases, 4 occurred following tube thoracostomy placement, 2 followed thoracotomy for lung resection, 2 were the result of esophageal operations, and 1 each followed a laparoscopic fundoplication, repair of a gastroschisis, development of a paronychia of the index finger, and minor chest wall trauma [2, 57]. Of these patients, 3 survived, leading to an overall mortality of 77% for 13 patients. Death most commonly resulted from multiple organ failure initiated by the septic challenge.
Wide surgical debridement of all necrotic and infected tissue is a central tenet in the successful management of patients with necrotizing fasciitis. Three patients [5, 8], including two survivors, required sufficiently extensive debridement to lead to entry into the pleural space. These were each managed with packing changes, resulting in granulation response and wound contracture. It is unclear as to how the defect in the thoracic cage was managed in the case of the other reported survivor [5]. In the case of the nonsurvivor [8], the authors reported that the thoracic defect was left open and involved in subsequent packing changes. Following further debridement, split-thickness skin grafts were performed. According to the authors description, this led to a lasting pleurocutaneous fistula although pleural symphysis was present. In our case, closure with polyglactin 910 mesh successfully provided a platform for dressing changes and extension of the granulation response. In our experience with patients who have had this absorbable mesh placed over open abdominal wounds and have been allowed to undergo granulation and wound contraction, we have found that the mesh encourages a hearty fibrotic reaction as it dissolves. The process usually takes 6 to 8 weeks. We assume a similar change took place in the chest wall. This is highly desirable because the rigidity and strength of the repaired segment should allow relative normalization of ventilatory mechanics. In addition, our clinical experience gathered while using this technique for closure of infected abdomens suggests that the mesh permits necessary white blood cell migration during the acute phase of the infection, permitting resolution of the infectious process.
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References
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McHenry C.R., Piotrowski J.J., Petrinic D., et al. Determinants of mortality for necrotizing soft tissue infections. Ann Surg 1995;221:558-565.[Medline]
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Urschel J.D., Takita H., Antkowiak J.G. Necrotizing soft tissue infections of the chest wall. Ann Thorac Surg 1997;64:276-279.[Abstract/Free Full Text]
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Giuliano A., Lewis F., Jr, Hadley K., Blaisdell F.W. Bacteriology of necrotizing fasciitis. Am J Surg 1977;134:52-57.[Medline]
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McHenry C.R., Malangoni M.A. Necrotizing soft tissue infections. In: Fry D.E., ed. Surgical infections. Boston: Little, Brown and Company, 1995:161-168.
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Viste A., Vindenes H., Gjerde S. Herniation of the stomach and necrotizing chest wall infection following laparoscopic Nissen fundoplication. Surg Endosc 1997;11:1029-1031.[Medline]
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Banwell P.E., Pereira J., Powell B.W. Symmetrical necrotizing chest wall infection following paronychia. J Accid Emerg Med 1998;15:58-66.[Abstract/Free Full Text]
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Hammainen P., Kostiainen S. Postoperative necrotizing chest wall infection. Scand Cardiovasc J 1998;32:243-245.[Medline]
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Urschel JD, Horan TA, Unruh HW. Comp Surg 1993;12:3739, 43.
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