J. Biomedical Science and Engineering, 2013, 6, 6-13 JBiSE http://dx.doi.org/10.4236/jbise.2013.612A002 Published Online December 2013 (http://www.scirp.org/journal/jbise/ ) Biomechanical aspects of catheter-related thrombophlebitis Oren Moshe Rotman * , Dalit Shav, Sagi Raz, Uri Zaretsky, Shmuel Einav Department of Biomedical Engineering, Tel Aviv University, Tel Aviv, Israel Email: * orenrotm@post.tau.ac.il Received 30 September 2013; revised 29 October 2013; accepted 12 November 2013 Copyright © 2013 Oren Moshe Rotman et al. This is an open access article distributed under the Creative Commons Attribution Li- cense, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. ABSTRACT Short peripheral catheters (SPCs) are the most com- mon intravenous devices used in medical practice. Short peripheral catheter thrombophlebitis (SPCT) is the most frequent complication associated with SPCs, causing discomfort and usually leading to removal of the catheter and insertion of a new one at a different site. The aim of this research was to explore whether biomechanical factors, in addition to biochemical factors, also play a role in the formation of thrombo- phlebitis. Hence, two of the biomechanical aspects of SPCT were investigated: the physical pressure load exerted by the SPC on the endothelial monolayer, and disturbances in the flow patterns due to the SPC. Endothelial activation was studied by subjecting hu- man umbilical vein endothelial cells (HUVEC) to a weight load of SPC pieces and measuring the release profile of von-Willebrand Factor (vWF) over time, using ELISA. vWF release was chosen as the measure for endothelial activation since it was the major com- ponent of the Weibel-Palade Bodies (WPBs), which underwent exocytosis by endothelial cells during acti- vation. Flow patterns were analyzed on a 3D compu- tational fluid dynamics (CFD) model of a brachio- cephalic vein with SPC. vWF release profiles were significantly higher in the HUVECs subjected to the load, indicating HUVEC activation. CFD simulations demonstrated a decrease in flow velocities along the catheter body, between the catheter and the vein, due to an enlarged boundary layer. Results indicate that the contact region between the SPC body and the vein wall can be partially responsible for SPCT develop- ment, and inflammatory and coagulatory processes initiated by stimulated endothelial cells may be am- plified due to disturbed blood flow. Keywords: Endothelial Activation; vWF; Thrombophlebitis; Phlebitis; Short Peripheral Catheters; Infusion; Intravenous Access; CFD 1. INTRODUCTION Short peripheral catheters (SPC) are the most widely used intravenous devices in medical practice today, par- ticularly in hospitals and intensive care units. The SPC is commonly inserted into veins of the upper extremities to administer fluids, medications and blood products, or for prophylaxis before procedures. Short peripheral catheter thrombophlebitis (SPCT) is the most frequent complica- tion associated with SPCs, with prevalence in hospital- ized patients ranging from 2.6% [1] to 77.5% [2]. This inflammatory process of the vein wall is characterized by pain, tenderness, warmth, erythema, swelling, and some- times palpable thrombosis of the cannulated vein. In the past, SPCT was thought to be initiated by infection from the insertion site, but studies of catheter tip cultures sug- gest it may be mediated or initiated by a noninfectious inflammatory process [1,3-6]. Moreover, SPCT symp- toms such as local swelling and erythema on the skin surface commonly appear along the venous track [7], making the catheter penetration wound not necessarily initiate the inflammatory process. These findings led us to hypothesize that the inflammatory process of SPCT is initiated by the interaction between the catheter body, the vein wall, and the blood flow. SPCT causes discomfort and usually results in re- moval of the catheter and insertion of a new one at a dif- ferent site. Repeated episodes can lead to venous access difficulties and more invasive procedures, such as central venous catheter placement. This usually results in delay- ed administration of parenteral medications, lengthened hospital stay and increased costs [6]. Several mecha- nisms of SPCT pathogenesis have been suggested, in- cluding vein wall injury combined with stasis and in- flammation that lead to thrombosis [8], and sterile in- flammation caused by chemical irritation of the endothe- * Corresponding author. OPEN ACCESS