Fibrin sheaths are a well-known complication of central venous catheters, with the earliest descriptions dating back to 1964 [2]. These sheaths can form as early as 24 h post-insertion and can encase the entire length of the catheter by 5–7 days [1, 3]. They usually arise at two sites of endothelial injury, namely at the venous entry site of the catheter as well as at the catheter tip, where there is contact with the venous wall [1]. Forauer et al. [5] described two microscopic patterns of histological changes, in which focal intimal injury and pericatheter thrombus formation were seen in short-term catheters, while smooth muscle proliferation, venous wall thickening with focal catheter attachment to the vessel wall, organization of thrombus and collagen formation were observed in long-term catheters.
These sheaths can be retained post-catheter removal and are sometimes calcified as reported by Krausz et al. They found that 21% of these fibrin sheaths remnants were in patients with end-stage renal disease, likely due to the larger diameter of the dialysis catheters, which increased the degree of traumatic contact with the venous wall as compared to the smaller caliber of CVCs and peripherally inserted central catheters (PICC) used for other purposes. These dialysis catheters were also typically left in situ for longer periods, predisposing to sheath formation [4]. In a study of tunneled dialysis catheter exchange and de novo placements by Shanaah et al. [6], they noted that fibrin sheath incidence was 47%. Matusik et al. [7] found 17 case reports of CVC-related fibrin sheaths, of which eight cases were in hemodialysis patients with retained calcified fibrin sheaths, some initially misinterpreted as a retained catheter tip. In this case, our patient had a history of multiple CVC insertions and exchanges as well as a long-term tunneled dialysis catheter which was left in situ for 2 years, increasing his risk of fibrin sheath formation and retention.
Imaging findings of fibrin sheaths on fluoroscopic catheter venography have been well described [8] and well known among radiologists. This is due to the common complication of fibrin sheaths causing catheter dysfunction, thus requiring catheter venography for further evaluation. However, not many may be familiar with the CT imaging features of retained catheter sheaths, causing diagnostic confusion especially when calcified as they may mimic a retained catheter fragments due to the hyperdense tubular configuration of the sheaths as seen in several case reports [9,10,11]. Commonly reported CT findings of calcified retained sheaths are an irregularly shaped discontinuous or interrupted tubular structure, similar to or nearing bone density with a patent lumen within, as well as with a diameter greater than expected for a CVC [4, 7, 10, 11]. In some cases, contrast material was seen to pass through the lumen [12]. The contrast material may sometimes be isodense to the sheath, making them inconspicuous on contrast-enhanced CT scan, and are therefore better visualized on non-contrasted scans [4, 7]. On the other hand, a fractured catheter would be seen as a continuous tubular structure, and due to the spatial resolution of CT scanners, the lumen of a retained catheter fragment may not be well-visualized, especially when the lumen is less than 2 mm. Therefore, Baciarello et al. recommended examining the presence or absence of a lumen as a criterion for differentiating a catheter from a sheath [11].
In our patient, the hyperdense tubular structure that was seen on the initial unenhanced CT thorax within the right brachiocephalic vein and SVC gave the impression of a retained catheter fragment adherent to the vessel wall at first glance (Fig. 1). However, on closer inspection, the hyperdense tubular structure was noted to have an average density of 600–800HU and appeared to be discontinuous and interrupted, with a visible lumen measuring 2.7 mm in maximum diameter. The overall outer diameter of this tubular structure measured approximately 10 mm, which is much larger than expected in comparison with the diameter of a 16-French permanent tunneled dialysis catheter. No contrast was seen within the lumen, and there was also concomitant stenosis and occlusion involving bilateral brachiocephalic veins near the confluence and the upper SVC. All these features therefore lead to the diagnosis of a retained calcified fibrin sheath in our patient. Retrospective analysis of the chest radiograph taken on admission showed evidence of the sheath at the right paratracheal region (Fig. 4).
It is unknown whether the fibrin sheath in our patient was calcified prior to catheter removal or whether the calcifications developed after being retained, as there was no previous CT done and we were unable to obtain his previous chest radiographs for comparison, due to the last catheter being removed 5 years ago. From previous case reports, calcifications of the sheaths were noted in hemodialysis patients with increased levels of serum calcium, phosphate and parathyroid hormones [3, 13]. Vascular calcifications may also be due to inflammatory cytokines, metabolic or genetic etiology [7]. Krausz et al. [4] observed calcification of a previously non-calcified sheath in one patient, proving that the sheath may become calcified after being retained. In our patient, his recent blood parameters were within normal range; however, we were unable to assess his old records to ascertain whether he had any previous derangement in his calcium and phosphate metabolism.
Central venous stenosis is a common problem among hemodialysis patients. They are more commonly associated with CVCs inserted into the subclavian vein as compared to the internal jugular veins and, however, may also occur without a history of previous catheter placement in up to 40% of patients [14, 15]. In patients with prior CVC insertions, endothelial injury and mechanical irritation by the catheters predispose to luminal narrowing of the central veins causing stenosis and occlusion [5, 16]. Retained fibrin sheaths with associated venous occlusions have been reported in cases on CT as well as on autopsy [1, 4, 5]. Our patient had a history of repeated cannulation to his right internal jugular vein likely causing recurrent vessel trauma with recurrent sheath formation, venous wall thickening and subsequent central venous occlusion. It is likely that this occlusion did not occur acutely, in view of the presence of well-established collateral channels in this patient. However, his acute symptoms of progressive facial and neck swelling which occurred only after revision of his AVF were likely attributed to the sudden increased in blood flow from the AVF, increasing blood flow through the collateral system. As the obstruction was at the level of the brachiocephalic and preazygos SVC, he had collateral drainage via the right superior intercostal veins and azygos veins.
Management of central venous stenosis may be conservative in asymptomatic cases. For patients who are symptomatic, depending on the degree of stenosis, balloon angioplasty with or without stenting may be performed. In our case, the degree of stenosis was severe and our patient was symptomatic; however, due to the sheath being calcified and adherent to the wall, balloon angioplasty was not a feasible option. He was referred for ligation of his left brachial AVF to relieve the symptoms of neck and facial swelling. At the time of this report, he is on regular hemodialysis via a long-term tunneled femoral catheter and remains well.
