Sundaram et al. reported the spectrum of CT findings and clinical outcomes among patients with thoracic aortic graft complications detected on CT [1]. CT-evident complications were identified in approximately 2.2% of the cases over a 7-year period, which suggests an extremely low complication rate. The most frequent type of CT-evident complication is the abnormal accumulation of low-attenuation material around the graft (51%), followed by collections of contrast material outside the graft (33%). PGS can be devastating as it can cause secondary graft infection, and PGS symptoms can vary depending on the site of formation. An asymptomatic mass [2], pain, acute limb ischemia secondary to graft limb compression, and respiratory distress have been reported [3].
Identifying PGS in the clinical setting is difficult, and the differential diagnoses include infection, pseudoaneurysm, postoperative hematoma, and lymphatic fluid collection. The accumulation of low-attenuation perigraft fluid is most often caused by infection, which must be ruled out. Bleeding because of anastomotic dehiscence without infection is a less frequent cause that is more frequently encountered in the early postoperative period and needs to be ruled out as well. In approximately 50% of the cases, the cause of low-attenuation perigraft fluid collection is not identified [1], and the patients remain asymptomatic. Kadakol et al. [3] defined PGS as a perigraft fluid collection present for >3 months after surgery, with a diameter ≥3.0 cm and a radiodensity ≤25 HU. The present case met all three of these criteria. The mechanism underlying PGS formation remains unclear, but it is hypothesized to be the result of postoperative seroma and/or inflammatory edema developing because of an allergic reaction to the aortic graft material. Yamamoto et al. [4] suggested that collagen-impregnated vascular grafts contain contaminants with endotoxins and (1-3) b-D-glucan, which may cause a sterile inflammatory response around the graft. Whether the graft serves as a predisposing factor for PGS formation is controversial. Knitted Dacron grafts were most frequently used, followed by polytetrafluoroethylene [5]. Kadakol et al. [3] reported that diabetes, smoking, anticoagulation, bifurcated graft reconstruction, and left flank retroperitoneal approach were independent risk factors for the development of PGS after the open surgical repair of AAA.
Although the success rate of surgical intervention is unclear because of the rarity of PGS, several cases of successful surgical intervention have been reported. Ohtake et al. [6] reported the successful endovascular therapy for PGS of the descending aorta. Kadakol et al. [3] reported that 4 (20%) of 20 patients with PGS required intervention after the open surgical repair of AAAs, and graft replacement with another type of graft was performed in 2 (10%) patients. One of the treatment options is drainage; however, because of recurrence, endovascular repair or surgery might be necessary in select cases. In the present case, the diagnosis was confirmed using a combination of radiodensity on preoperative CT, bacterial culturing, and laboratory and histological examinations. The cause of a gradually expanding PGS after repair of the thoracic aorta remains unknown; however, we believe that applying fibrin glue to the graft surface and wrapping a new graft around it prevents the recurrence of fluid accumulation around the prosthetic graft.
Physicians should be aware that chronic expanding mediastinal seroma with Dacron grafts is one of the rare postoperative complications of thoracic aortic surgery. Applying fibrin glue to the graft surface might effectively prevent the recurrence of PGS.