DOI: 10.1148/rg.245035169
RadioGraphics 2004;24:1472-1476
© RSNA, 2004
Necrotizing Fasciitis1
J. Brett Fugitt, MD,
Michael L. Puckett, MD,
Michael M. Quigley, MD, PhD and
Stewart M. Kerr, MD
1 From the Departments of Radiology (J.B.F., M.L.P.), Pathology (M.M.Q.), and Orthopedic Surgery (S.M.K.), Naval Medical Center, 34800 Bob Wilson Dr, San Diego, CA 92134. Received July 21, 2003; revision requested August 28 and received April 26, 2004; accepted April 29. All authors have no financial relationships to disclose. Address correspondence to J.B.F. (e-mail: coleybear@cox.net).
Index Terms: Extremities, abnormalities, 44.249 • Fasciitis, 44.249 • Soft tissues, infection, 44.249
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History
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A 57-year-old non–insulin-dependent diabetic man presented to the emergency department with right anterolateral thigh pain and malaise. He denied experiencing trauma. Physical examination revealed a warm and focally swollen right upper leg that was tender at palpation. The overlying skin was mottled (Fig 1). He was tachycardiac and mildly febrile with a temperature of 100.3°F (38.0°C). Laboratory studies revealed a leukocythemia with a white blood cell count of 39.7 x 103/mm3 (39.7 x 103/µL) and mild acute renal failure as indicated by a serum creatinine level of 2.4 mg/dL (212 µmol/L). Results of ultrasound (US) performed for suspected deep venous thrombosis were negative. Plain radiographs of the femur were normal.
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Imaging Findings
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Initial imaging with computed tomography (CT) was performed without contrast material due to the patient’s acute renal failure. CT images revealed skin thickening and increased attenuation of the subcutaneous fat with both subcutaneous and intermuscular stranding. Crescentic subfascial fluid collections were seen (Fig 2). No air or discrete abscess was identified. Some muscle groups were thickened with increased attenuation, suggesting edema.
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Figure 2. Selected axial nonenhanced CT image of the upper right thigh (soft-tissue window) shows skin thickening with increased attenuation and subcutaneous and intermuscular stranding. Crescentic subfascial fluid collections are seen. Increased reticular attenuation is seen in the subcutaneous fat. The rectus femoris (RF) and the remaining muscles have normal attenuation.
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Subsequent imaging with magnetic resonance (MR) was performed (Fig 3). T2-weighted sequences showed subcutaneous and intramuscular edema in a reticulated pattern as well as subfascial and interfascial crescentic fluid collections. T1-weighted images were only subtly abnormal with loss of muscle texture and a crescent of increased signal intensity in the vastus lateralis muscle, compatible with intramuscular hemorrhage.
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Figure 3a. (a) Axial nonenhanced T1-weighted MR image obtained with fat saturation shows subtle diffusely increased signal intensity in the vastus lateralis (VL) and vastus intermedius (VI) muscles relative to that in the rectus femoris (RF). The crescentic rim of increased signal intensity around the vastus lateralis is compatible with hemorrhage. Reticular increased signal intensity is seen in the subcutaneous fat. (b) Axial T1-weighted MR image obtained with fat saturation after administration of gadolinium contrast material shows subtle enhancement of the vastus lateralis (VL) and vastus intermedius (VI) with relative sparing of the rectus femoris (RF). The enhancement of the deep fascia and subcutaneous fat is not as distinct as on the T2-weighted image (c). (c) Axial T2-weighted fast spin-echo MR image of the proximal right thigh obtained with fat saturation shows increased signal intensity in the deep fascia of the anterolateral thigh and subtle increased signal intensity in the vastus lateralis (VL) and vastus intermedius (VI) relative to that in the rectus femoris (RF). There is overlying reticular increased signal intensity in the subcutaneous fat. These signal intensity abnormalities are more conspicuous and demonstrate the extent of involved tissue better than on the contrast-enhanced T1-weighted image (b).
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Figure 3b. (a) Axial nonenhanced T1-weighted MR image obtained with fat saturation shows subtle diffusely increased signal intensity in the vastus lateralis (VL) and vastus intermedius (VI) muscles relative to that in the rectus femoris (RF). The crescentic rim of increased signal intensity around the vastus lateralis is compatible with hemorrhage. Reticular increased signal intensity is seen in the subcutaneous fat. (b) Axial T1-weighted MR image obtained with fat saturation after administration of gadolinium contrast material shows subtle enhancement of the vastus lateralis (VL) and vastus intermedius (VI) with relative sparing of the rectus femoris (RF). The enhancement of the deep fascia and subcutaneous fat is not as distinct as on the T2-weighted image (c). (c) Axial T2-weighted fast spin-echo MR image of the proximal right thigh obtained with fat saturation shows increased signal intensity in the deep fascia of the anterolateral thigh and subtle increased signal intensity in the vastus lateralis (VL) and vastus intermedius (VI) relative to that in the rectus femoris (RF). There is overlying reticular increased signal intensity in the subcutaneous fat. These signal intensity abnormalities are more conspicuous and demonstrate the extent of involved tissue better than on the contrast-enhanced T1-weighted image (b).
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Figure 3c. (a) Axial nonenhanced T1-weighted MR image obtained with fat saturation shows subtle diffusely increased signal intensity in the vastus lateralis (VL) and vastus intermedius (VI) muscles relative to that in the rectus femoris (RF). The crescentic rim of increased signal intensity around the vastus lateralis is compatible with hemorrhage. Reticular increased signal intensity is seen in the subcutaneous fat. (b) Axial T1-weighted MR image obtained with fat saturation after administration of gadolinium contrast material shows subtle enhancement of the vastus lateralis (VL) and vastus intermedius (VI) with relative sparing of the rectus femoris (RF). The enhancement of the deep fascia and subcutaneous fat is not as distinct as on the T2-weighted image (c). (c) Axial T2-weighted fast spin-echo MR image of the proximal right thigh obtained with fat saturation shows increased signal intensity in the deep fascia of the anterolateral thigh and subtle increased signal intensity in the vastus lateralis (VL) and vastus intermedius (VI) relative to that in the rectus femoris (RF). There is overlying reticular increased signal intensity in the subcutaneous fat. These signal intensity abnormalities are more conspicuous and demonstrate the extent of involved tissue better than on the contrast-enhanced T1-weighted image (b).
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Pathologic Evaluation
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The surgical resection specimen consisted of a right leg amputation from the femoral head to the foot (Fig 4). Deep histologic sections of skeletal muscle taken from multiple sites demonstrated expansion of the fibrous septa by edema, mixed inflammatory cell infiltrate, and early fibroblastic proliferation. Multiple foci of muscle fiber dropout were identified. The presence of early fibroblastic proliferation suggested the time course of this process to be at least 1–2 weeks in duration (Fig 5).
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Figure 5a. (a) Low-power photomicrograph (original magnification, x150; hematoxylin-eosin stain) shows expansion of the inter- and intrafascicular fibrous septa (*) surrounding skeletal muscle bundles. The expanded fibrous septa are edematous and contain a mixed inflammatory infiltrate and early fibroblastic proliferation, which is most prominent on the left side of the image. A small lymphoid collection is also present (arrow). (b) High-power photomicrograph (original magnification, x400; hematoxylin-eosin stain) shows atrophy of skeletal muscle (MF) and a mixed inflammatory infiltrate, which consists of lymphocytes (L), plasma cells (PC), neutrophils (N), and rare eosinophils (E). There is also early fibroblastic proliferation.
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Figure 5b. (a) Low-power photomicrograph (original magnification, x150; hematoxylin-eosin stain) shows expansion of the inter- and intrafascicular fibrous septa (*) surrounding skeletal muscle bundles. The expanded fibrous septa are edematous and contain a mixed inflammatory infiltrate and early fibroblastic proliferation, which is most prominent on the left side of the image. A small lymphoid collection is also present (arrow). (b) High-power photomicrograph (original magnification, x400; hematoxylin-eosin stain) shows atrophy of skeletal muscle (MF) and a mixed inflammatory infiltrate, which consists of lymphocytes (L), plasma cells (PC), neutrophils (N), and rare eosinophils (E). There is also early fibroblastic proliferation.
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Discussion
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Necrotizing fasciitis is a rapidly progressive and often fatal infection of the soft-tissue fascia deep to the skin but superficial to the muscles. It was first described by Joseph Jones, an American army surgeon during the American Civil War, and was popularized in the lay media during the 1980s after an increase in prevalence said to be caused by "flesh-eating bacteria" (1). The disease may afflict the immunocompetent; however, elderly patients and those with impaired immunity are at increased risk (2). This includes intravenous drug and alcohol abusers, diabetics, patients with human immunodeficiency virus or leukemia, and those undergoing chemotherapy or taking immunosuppressive medication (3,4). Predisposing factors include underlying infections such as diverticulitis, furuncles, minor trauma, surgery, or even insect bites (3,5). Factors associated with a poor outcome include diabetes mellitus, alcoholism, peripheral vascular disease, obesity, and old age (5). The mortality rate may be as high as 30%–70% (6), with death being due to sepsis, respiratory failure, kidney failure, or multi–organ system failure (2,5).
The most common type of necrotizing fasciitis is a polymicrobial infection with both aerobic and anaerobic organisms such as Clostridium, Proteus, Escherichia coli, Bacteroides, and Enterobacteriaceae (3). This form of the disease is often seeded from underlying infections such as diverticulitis (7). A second form of the disease is caused by group A streptococci, the "flesh-eating bacteria," and is seen in approximately 10% of cases (3,6). Toxic shock syndrome may complicate this latter form (6).
The clinical presentation is often nonspecific, and a high clinical suspicion is therefore needed for timely diagnosis. Patients may present with systemic complaints of fever and malaise and only vague localizing symptoms (7). If treatment is delayed, patients invariably progress to sepsis, developing tachycardia, hypotension, and acute renal failure (4). The overlying skin may appear normal, or the local examination findings may be subtle and mistaken for those of cellulitis (2). The infection is not walled off as in an abscess and therefore lacks a clear boundary, making palpation challenging (8). This lack of a walled-off boundary accounts for both the rapid spread of disease and the difficulty in clinical diagnosis (7). Crepitus due to superficial fascial emphysema is only rarely palpable (5). However, the overlying skin is classically warm and indurated, so-called "wooden skin," with mottled, purple patches (3,8). Extreme pain followed by anesthesia suggests the diagnosis (3).
The rapidity of spread and the subsequent deterioration of the patient’s condition require rapid diagnosis, which may be facilitated by radiology. The disease is a surgical emergency with high mortality; therefore, imaging studies should not delay surgical intervention (6). Plain radiography, CT, MR imaging, and even US may suggest the radiologic diagnosis.
The most common plain radiographic findings are similar to those of cellulitis, with increased soft-tissue thickness and opacity (4). Frequently, plain radiographs are normal until the infection and necrosis are advanced (5). The characteristic finding is gas in the soft tissues, although this is seen in only a minority of cases (9).
CT characteristics correlate with the pathologic findings of liquefied, necrotic tissue and inflammation resulting from bacterial exotoxins released in the fascial layers (2). The CT hallmark of necrotizing fasciitis is soft-tissue air associated with fluid collections within the deep fascia, although this finding is inconstant (1,2). Also evident at CT are thickening and enhancement of one or both of the superficial and deep fascial layers. The subcutaneous fat may be similarly affected (1,2). While fascial fluid collections are typically nonfocal, abscesses may be seen (4). Reactive lymphadenopathy is also commonly present (2). Since many patients present with acute renal failure, contrast material administration may be contraindicated. Potential advantages of CT include the ability to detect underlying infectious sources such as diverticulitis or underlying bony involvement (4,5). CT may also demonstrate serious complications such as vascular rupture complicating tissue necrosis (2).
Liquefactive tissue necrosis and inflammatory edema both create fascial fluid that is detected with MR imaging as abnormally increased signal intensity on T2-weighted images and variably increased signal intensity on T1-weighted images along thickened deep fascial planes (4). In general, fat-suppressed T2-weighted imaging has been found to display inflammatory changes better than fat-suppressed gadolinium-enhanced T1-weighted imaging (10). Gas bubbles, if present, appear as focal signal voids on both T1- and T2-weighted images (4). The subcutaneous tissues may have reticular increased signal intensity, similar to cellulitis. Unlike cellulitis, however, the deep fascia is also involved (1). Since both infected necrotic tissue and noninfected edematous tissue have a similar appearance on MR images, the extent of infection may be overestimated (4,10). Gadolinium contrast material is not necessary for diagnosis, although it may be helpful in detecting abscesses or in distinguishing joint effusion from surrounding inflammation (10). The degree of contrast enhancement may cause the extent of disease to be underestimated due to hypoperfusion and tissue necrosis (10).
US has been most useful in the pediatric age group. Key sonographic findings include distorted and thickened fascial planes with turbid fluid accumulation in the fascial layers and subcutaneous edema (11). The examination may be limited by soft-tissue gas, although this finding may be of diagnostic benefit (5,6). US may also be used to guide fluid aspiration (11).
The treatment for necrotizing fasciitis is prompt surgical fasciotomy and débridement of the necrotic tissue (7). These patients are seriously ill, and their postoperative care should be managed in an intensive care setting since fluid resuscitation, pressor support, cardiac monitoring, and ventilator support may be necessary (2,3,5). Broad-spectrum antibiotic coverage should be maintained until the causative organisms have been identified (3).
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Conclusions
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Necrotizing fasciitis is a rapidly progressive soft-tissue infection with a high mortality rate if treatment is delayed. Rapid diagnosis and prompt surgical débridement are necessary to ensure a good outcome. Plain radiography, US, and cross-sectional imaging techniques have all been used to expedite the diagnosis. Whichever modality is employed, the goal of imaging is to hasten the diagnosis and treatment; treatment should not be delayed to facilitate imaging.
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References
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- Donnelly L, Frush D, O’Hara S, Bissett G. Necrotizing fasciitis: an atypical cause of acute abdomen in an immunocompromised child. Pediatr Radiol 1998; 28:109-111.[CrossRef][Medline]
- Becker M, Zbaren P, Hermans R, et al. Necrotizing fasciitis of the head and neck: role of CT in diagnosis and management. Radiology 1997; 202:471-476.[Abstract/Free Full Text]
- Callahan E, Adal K, Tomecki K. Cutaneous (non HIV) infections. Dermatol Clin 2000; 18:497-508.[CrossRef][Medline]
- Struk D, Munk P, Lee M, Ho S, Worsley D. Imaging of soft tissue infections. Radiol Clin North Am 2001; 39:277-301.[CrossRef][Medline]
- Walshaw C, Deans H. CT findings in necrotizing fasciitis: a report of four cases. Clin Radiol 1996; 51:429-432.[CrossRef][Medline]
- Cardinal E, Bureau N, Aubin B, Chem R. Role of ultrasound in musculoskeletal infections. Radiol Clin North Am 2001; 39:191-199.[CrossRef][Medline]
- Wessels M. Streptococcal infections. In: Isselbacher K, Braunwald E, Wilson J, Martin J, Fauci A, Kasper D, eds. Harrison’s principles of internal medicine. 13th ed. New York, NY: McGraw Hill, 1994; 617-623.
- Alexander J, Dellinger P. Surgical infections and choice of antibiotics. In: Sabiston D, eds. Textbook of surgery. 14th ed. Philadelphia, Pa: Saunders, 1991; 221-236.
- Rehman J, Kaynan A, Samadi D, Fleischman J. Air on radiography of perirenal necrotizing fasciitis indicates testis involvement. J Urol 1999; 162:2101.[CrossRef][Medline]
- Miller T, Randolph D, Staron R, Feldman F, Cushin S. Fat-suppressed MRI of musculoskeletal infection: fast T2-weighted techniques versus gadolinium-enhanced T1-weighted images. Skeletal Radiol 1997; 26:654-658.[CrossRef][Medline]
- Chao H, Kong M, Lin T. Diagnosing necrotizing fasciitis in children. J Ultrasound Med 1999; 18:277-281.[Abstract]
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History
Imaging Findings
