TITLE:
Biomechanical aspects of catheter-related thrombophlebitis
AUTHORS:
Oren Moshe Rotman, Dalit Shav, Sagi Raz, Uri Zaretsky, Shmuel Einav
KEYWORDS:
Endothelial Activation; vWF; Thrombophlebitis; Phlebitis; Short Peripheral Catheters; Infusion; Intravenous Access; CFD
JOURNAL NAME:
Journal of Biomedical Science and Engineering,
Vol.6 No.12A,
December
17,
2013
ABSTRACT: Short
peripheral catheters (SPCs) are the most common 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 thrombophlebitis.
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 human 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 component of the Weibel-Palade Bodies (WPBs),
which underwent exocytosis by endothelial cells during activation. Flow
patterns were analyzed on a 3D computational fluid dynamics (CFD) model of a
brachiocephalic 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 development, and inflammatory and coagulatory
processes initiated by stimulated endothelial cells may be amplified due to
disturbed blood flow.