Encapsulated fat necrosis is a benign condition that was first described in 1975 by Schmidt-Hermes and Loskant,1 with further characterization by Przyjemski and Schuster in 1977.2 Since these initial reports, a variety of different names have been alternatively used in the literature to describe these lesions. These terms include nodular-cystic fat necrosis, mobile encapsulated lipoma, encapsulated necrosis, or posttraumatic fat necrosis.3,4 The common pathogenesis is hypothesized to result from rapid infarction of adipose tissue lobules secondary to trauma and interruption of blood supply.3 This process causes the separation of necrotic adipose from the surrounding tissue and elicits an inflammatory cellular response to tissue injury coordinated by macrophage infiltration.5 This initial injury phase is followed by a fibrocellular response and the ultimate formation of a fibrous pseudomembrane or capsule that forms around the coalesced necrotic fat. This fibrous capsule creates a cleavage plane between the surrounding tissues and renders these lesions mobile. Given that these encapsulated nodules are sequestered from the blood supply, they cannot be reabsorbed and may accumulate lamellar units of fibrosis over time. The interior contents of the fibrous capsule contain necrotic fatty tissue with occasional degrees of degenerative changes, including dystrophic calcifications.
The characterization of encapsulated fat necrosis has been limited by the scarcity of cases reported in the literature. Almost all reported cases have occurred in the extremities within exposed areas that are prone to frequent or repeated blunt trauma, such as the subcutaneous tissues of the legs, arms, elbows, thighs, and back.6 These lesions have a variable appearance on radiographic imaging and may appear either solid or cystic. Histologically, fibrous septa are found to encapsulate internal contents that may include necrotic adipose tissue, inflammatory cell infiltrates, or calcification, which is thought to represent the end stage of formation.6 When these lesions are surgically removed, no recurrences within the surgical bed have been reported.4
To our knowledge, our finding is one of the first reported cases of encapsulated fat necrosis that presented as a free-floating mass within the intra-abdominal cavity of a human. Interestingly, however, this condition is found to be an occasional incidental finding in cattle when they are taken for slaughter and the abdominal contents are examined.7 In 1956, Dockerty et al8 described the pathologic characteristics of detached epiploic appendages in the abdominal cavity that developed into free-floating nodules, designated as “loose bodies” by the authors. The encapsulation of infarcted epiploic fat may in fact be more prevalent than has been reported but nevertheless remains asymptomatic and undetected. Judging from the extent of lamellar septa of fibrosis that encapsulated the necrotic fat within our specimen, it likely had been in the process of formation for many years without causing any symptoms.
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Correspondence: Dr Choti, Department of Surgery, Johns Hopkins University School of Medicine, 600 N Wolfe St, Blalock 665, Baltimore, MD 21287 (email@example.com).
Accepted for Publication: April 6, 2011.
Author Contributions:Study concept and design: Brooke and Choti. Acquisition of data: Brooke and Choti. Analysis and interpretation of data: Brooke and Choti. Drafting of the manuscript: Brooke. Critical revision of the manuscript for important intellectual content: Brooke and Choti. Administrative, technical, and material support: Choti. Study supervision: Choti.
Financial Disclosure: None reported.
Image of the Month—Diagnosis. Arch Surg. 2011;146(12):1448. doi:10.1001/archsurg.146.12.1448
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