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Case Report |
1 Department of Radiology, Hospital Vall d'Hebron, Universitat Autonoma Pg. Vall
d'Hebron 119-129, Barcelona 08035, Spain.
2 Department of Radiology, Hospital Universitario Dr. Peset, Valencia,
Spain.
Received August 19, 2004;
revised October 19, 2004;
Address correspondence to V. Pineda
(victor{at}pineda.com.es).
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We present two cases of epipericardial fat necrosis studied with CT. In both cases, CT clearly showed that the lesion was located anterior to the pericardium—that is, in the epipericardial fat, not the pericardial fat, as has been previously described. On the basis of the surgical results of previously reported cases, we believe that the term "pericardial fat" is a misnomer, and for this reason, we will use the term "epipericardial fat" in this article.
Of our two patients, one underwent surgery. The other patient was followed with serial CT. To our knowledge, this is the first reported case of the evolution of acute epipericardial fat necrosis. We believe that the clinical and radiologic findings suffice to suggest the diagnosis of epipericardial fat necrosis, for which conservative treatment is indicated.
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The pathogenesis of epipericardial fat necrosis is unknown. Trauma and ischemia are associated with fat necrosis in systemic adipose tissue. Jackson et al. [1] suggested that obesity could be a predisposing factor, but later studies have shown that it also may occur in thin individuals [2–4]. Acute torsion has been proposed as the cause of ischemic necrosis of the epipericardiac fat, although the presence of a vascular pedicle has been described in only two cases [5]. It has also been hypothesized that increased thoracic pressure related to a Valsalva's maneuver may produce an elevation of capillary pressure that could lead to hemorrhagic necrosis.
The pathologic features are similar to those found in fat necrosis in epiploic appendagitis, omentum, and breast [1]. They depend on the age of the lesion. In the initial phases, there are findings of fat necrosis with varying degrees of inflammatory reaction. Within days, a chronic inflammatory infiltrate appears. In advanced lesions, foreign-body giant cells, calcium salts, and blood pigments are present. Finally, the lesion resolves into scar tissue or is walled off by a dense collagenous capsule [1, 3, 6].
Epipericardial fat necrosis debuts with acute chest pain, which is usually self-limiting and sometimes recurs several days later. Symptoms usually last several weeks, although there is one case in which the symptoms persisted for 1 year [7].
The diagnosis of epipericardial fat necrosis is rarely established before surgery. Posteroanterior chest radiography usually shows a paracardiac opacity, occurring predominantly on the left side. Associated pleural effusion may occur. Excluding our patients, only three cases of epipericardial fat necrosis studied on CT have, to our knowledge, been reported [2, 3, 6], none of which has been reported in the radiology literature. In none of these cases was the location of the lesions specified (intra- or extrapericardial), nor was there any mention of accompanying pericardial thickening. In all cases, the area of necrosis appeared as an encapsulated fat-density mass that was indistinguishable from other fat-containing lesions, such as lipoma or liposarcoma. The inflammatory infiltration of the necrotic fat may increase the density of the fat or create stranding, as in our second patient. The presence of strands inside the epipericardial fat is a finding that has also been described in other entities with fat necrosis, such as appendagitis and omental torsion [8, 9]. This finding may suggest a malignant lesion, such as a liposarcoma, to those who are not aware of the appearance of epipericardial necrosis.
The higher spatial resolution of modern CT scanners allows better characterization of the lesion and orientation of the diagnosis. The main CT features in epipericardiac fat necrosis are an encapsulated fatty lesion with inflammatory changes such as dense strands, thickening of the adjacent pericardium, or both. Together with acute chest pain, these findings form a triad highly suggestive of the diagnosis of fat necrosis. CT is also helpful for showing the location of the lesion anterior to the pericardium, indicating that the necrosis occurs in the epipericardium, indicating that the necrosis occurs in the mediastinal fat adjacent to the parietal pericardium rather than the pericardium as has been mentioned in all the previous cases. A review of the surgical findings of previously reported cases [1–7] shows that they either describe or imply that the affected fat is outside the parietal pericardium and not between both pericardial layers (true pericardial fat). We believe that the term "pericardial fat" is a misnomer carried over from initial publications and should be replaced by the term "epipericardial fat."
Since Jackson et al. [1] described epipericardial fat necrosis for the first time in 1957, only 19 cases have been reported, to our knowledge. All the patients underwent surgical treatment to confirm the diagnosis and rule out a possible malignant process. In our first case, the acute onset of the condition and the involution of the abnormal findings on radiologic follow-up (2 months) enabled us to rule out neoplastic disease. Although we do not have pathologic confirmation, we believe that the radiologic findings and the subsequent course of the condition allow us to establish the diagnosis of epipericardial fat necrosis with a high degree of confidence.
Although epipericardial fat necrosis is an uncommon entity, we believe it is important for the radiologist to be familiar with its features because the clinical and radiologic characteristics suggest a presumptive diagnosis, thereby avoiding more aggressive techniques. Because of its benign, self-limited nature, conservative treatment is indicated, as is done in cases of abdominal epiploic appendagitis.
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