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Central vein stenosis associated with hemodialysis access

Author
Gerald A Beathard, MD, PhD
Section Editors
Steve J Schwab, MD
John F Eidt, MD
Joseph L Mills, Sr, MD
Deputy Editor
Kathryn A Collins, MD, PhD, FACS

INTRODUCTION

A common problem in the management of patients undergoing hemodialysis is central vein stenosis (CVS) or occlusion. An important goal of all physicians who care for patients with severe renal dysfunction should be to preserve and protect the central veins, a task that is not easily accomplished. The development of this problem in the dialysis patient is a serious issue and it has a greater impact compared with stenosis of a peripheral vein because the central veins represent the final common pathway for blood flow from the periphery to the heart. If central stenosis progresses, arteriovenous hemodialysis vascular access is frequently lost. In addition, the development of central vein obstruction obviates the possibility of creating a new vascular access on the affected side. An unfortunate consequence of the loss of central vein patency for the patient is diminished life-expectancy.

Central vein stenosis associated specifically with hemodialysis access is reviewed here. General issues related to catheter-induced upper extremity venous thrombosis are reviewed separately. Thrombosis observed in patients with hemodialysis arteriovenous fistulas and grafts is reviewed separately. (See "Catheter-related upper extremity venous thrombosis" and "Hemodialysis arteriovenous graft dysfunction and failure".)

ETIOLOGY

Although the precise mechanisms by which central vein stenosis (CVS) occurs are not known, current concepts in its pathophysiology follow the response to vessel injury model, emphasizing the process of trauma, inflammation, intimal hyperplasia, and a fibrotic response. It is very likely that the exact mechanism can vary depending on the situation and may be multifactorial in many cases. Regardless of the inciting cause, the end result is the same. There is an upregulation of proinflammatory transcription factors and profibrotic genes, which in turn causes smooth muscle proliferation and thickening of the venous intima. The resulting venous outflow obstruction causes venous hypertension and threatens fistula and arm function. Certain inferences can be drawn from factors that are associated with the pathophysiology of central vein stenosis.

Vein injury – Central vein stenosis in the dialysis patient is most commonly associated with the presence of an intraluminal foreign body, either a central venous catheter (CVC) or the leads associated with a cardiac implantable electronic device (CIED). These lie in direct contact with the wall of the central veins and the constant movement of these associated with the dual processes of breathing and the cardiac cycle causes endothelial injury. Pathological examinations of central veins obtained at autopsy have shown that even short-term catheters are associated with foci of local intimal injury with endothelial denudation and adherent thrombus [1]. This injury appears to be aggravated if the route followed by the device is characterized by one or more curves, accounting for a higher incidence of central vein stenosis with subclavian or left internal jugular vein placement [2-4].

Inflammation – Data suggest that inflammation plays a role in CVS. The pathology associated with this lesion is characterized by neointimal hyperplasia [1]. This is a common response to vessel injury and is closely related to vessel injury and inflammation [5-7]. There is also an increased incidence of central vein stenosis in patients having had catheter-related infection [8,9]. Although not shown to be directly related to CVS, the mere presence of a CVC in the absence of infection has been shown to be associated with an increased level of systemic inflammation as indicated by increases in inflammatory markers [10].

                          

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Literature review current through: Nov 2016. | This topic last updated: Fri Oct 23 00:00:00 GMT+00:00 2015.
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