Andrew R Forauer1, Constantine Theoharis. 1. Section of Vascular/Interventional Radiology, Department of Radiology, B1D 530, University of Michigan Medical Center, 1500 E. Medical Center Drive, Ann Arbor, Michigan 48109-0030, USA. forauer@umich.edu
Abstract
PURPOSE: Central venous catheter dysfunction can be caused by thrombosis (of the catheter or vessel itself), fibrin sheath formation, or infection. These sequelae can lead to costly interventions, loss of the access device, or loss of access sites in as many as one-third of patients. This study examined the histologic changes in the access vein and superior vena cava wall that is adjacent to central venous catheters in humans. MATERIALS AND METHODS: The access vein, brachiocephalic vein, and superior vena cava were excised en bloc at autopsy from six patients with central venous catheters. The specimens were processed and stained with hematoxylin and eosin. The specimens were examined for histologic changes in the vein wall adjacent to the catheters, changes in the intima, and the presence of associated thrombus. RESULTS: Three catheters had been in place <14 days (short term), and three for >90 days (long term). Two microscopic patterns were observed. The short-term catheters displayed foci of local intimal injury with endothelial denudation and a layer of adherent thrombus. The second pattern, seen in the long-term catheters, consisted of smooth muscle cell proliferation leading to vein wall thickening. Focal areas of catheter attachment to the vein wall, composed of thrombus in varying stages of organization, collagen, and endothelial cells, were also observed. CONCLUSIONS: After short-term catheter placement, focal areas of endothelial injury were seen in the vein wall adjacent to the catheter. Associated thrombus may or may not be present. Long-term catheters displayed vein wall thickening and bridges from the vein wall to the catheter. These observations represent a progressive reaction of the human vein wall to access devices.
PURPOSE: Central venous catheter dysfunction can be caused by thrombosis (of the catheter or vessel itself), fibrin sheath formation, or infection. These sequelae can lead to costly interventions, loss of the access device, or loss of access sites in as many as one-third of patients. This study examined the histologic changes in the access vein and superior vena cava wall that is adjacent to central venous catheters in humans. MATERIALS AND METHODS: The access vein, brachiocephalic vein, and superior vena cava were excised en bloc at autopsy from six patients with central venous catheters. The specimens were processed and stained with hematoxylin and eosin. The specimens were examined for histologic changes in the vein wall adjacent to the catheters, changes in the intima, and the presence of associated thrombus. RESULTS: Three catheters had been in place <14 days (short term), and three for >90 days (long term). Two microscopic patterns were observed. The short-term catheters displayed foci of local intimal injury with endothelial denudation and a layer of adherent thrombus. The second pattern, seen in the long-term catheters, consisted of smooth muscle cell proliferation leading to vein wall thickening. Focal areas of catheter attachment to the vein wall, composed of thrombus in varying stages of organization, collagen, and endothelial cells, were also observed. CONCLUSIONS: After short-term catheter placement, focal areas of endothelial injury were seen in the vein wall adjacent to the catheter. Associated thrombus may or may not be present. Long-term catheters displayed vein wall thickening and bridges from the vein wall to the catheter. These observations represent a progressive reaction of the human vein wall to access devices.
Authors: Douglas M Silverstein; Scott O Trerotola; Timothy Clark; Garth James; Wing Ng; Amy Dwyer; Marius C Florescu; Roman Shingarev; Stephen R Ash Journal: Clin J Am Soc Nephrol Date: 2018-10-11 Impact factor: 8.237
Authors: Jeremías Bayón; María Martín; José Manuel García-Ruíz; Carmen Rodríguez Journal: Int J Cardiovasc Imaging Date: 2010-05-04 Impact factor: 2.357