Biomechanical aspects of catheter-related thrombophlebitis


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.


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Rotman, O. , Shav, D. , Raz, S. , Zaretsky, U. and Einav, S. (2013) Biomechanical aspects of catheter-related thrombophlebitis. Journal of Biomedical Science and Engineering, 6, 6-13. doi: 10.4236/jbise.2013.612A002.

Conflicts of Interest

The authors declare no conflicts of interest.


[1] Malach, T., Jerassy, Z., Rudensky, B., et al. (2006) Prospective surveillance of phlebitis associated with peripheral intravenous catheters. American Journal of Infection Control, 34, 308-312.
[2] Lundgren, A., Wahren, L.K. and Ek, A.C. (1996) Peripheral intravenous lines: Time in situ related to complications. Journal of intravenous nursing, 19, 229-238.
[3] Woodhouse, C.R. (1980) Infusion thrombophlebitis: The histological and clinical features. Annals of The Royal College of Surgeons of England, 62, 364-368.
[4] Cornely, O.A., Bethe, U., Pauls, R. and Waldschmidt, D. (2002) Peripheral Teflon catheters: Factors determining incidence of phlebitis and duration of cannulation. Infection Control and Hospital Epidemiology, 23, 249-253.
[5] Lanbeck, P., Odenholt, I. and Paulsen, O. (2002) Antibiotics differ in their tendency to cause infusion phlebitis: A prospective observational study. Scandinavian Journal of Infectious Diseases, 34, 512-519.
[6] Tagalakis, V., Kahn, S.R., Libman, M. and Blostein, M. (2002) The epidemiology of peripheral vein infusion thrombophlebitis: A critical review. American Journal of Medicine, 113, 146-151.
[7] Higginson, R. and Parry, A. (2011) Phlebitis: Treatment, care and prevention. Nursing Times, 107, 18-21.
[8] Tagalakis, V., Kahn, S.R., Correa, J.A., et al. (2007) Thrombophilia in short peripheral catheter thrombophlebitis. Thrombosis Research, 119, 587-592.
[9] Lanbeck, P., Odenholt, I. and Riesbeck, K. (2004) Dicloxacillin and erythromycin at high concentrations increase ICAM-1 expression by endothelial cells: A possible factor in the pathogenesis of infusion phlebitis. Journal of Antimicrobial Chemotherapy, 53, 174-179.
[10] Lewis, G.B. and Hecker, J.F. (1985) Infusion thrombophlebitis. British Journal of Anaesthesia, 57, 220-233.
[11] Subrahmanyam, M. (1989) Infusion thrombophlebitis— Histological and bacteriological study. Indian Journal of Medical Sciences, 43, 231-234.
[12] Wagner, D.D. and Frenette, P.S. (2008) The vessel wall and its interactions. Blood, 111, 5271-5281.
[13] Jesty, J., Yin, W., Perrotta, P. and Bluestein, D. (2003) Platelet activation in a circulating flow loop: Combined effects of shear stress and exposure time. Platelets, 14, 143-149.
[14] Albayrak, R., Yuksel, S., Colbay, M., et al. (2007) Hemodynamic changes in the cephalic vein of patients with hemodialysis arteriovenous fistula. Journal of Clinical Ultrasound: JCU, 35, 133-137.
[15] Kamm, R.D. and Pedley, T.J. (1989) Flow in collapsible tubes: A brief review. Journal of Biomechanical Engineering, 111, 177-179.
[16] Yaniv, S., Halpern, P., Aladgem, D., Zaretsky, U. and Elad, D. (2000) In vitro model of intravenous fluid administration: Analysis of vein resistance to rapid fluid delivery. Medical Engineering & Physics, 22, 395-404.
[17] Henry, W.R., William, E.M. and Eugene, B.F.J. (1944) The influence of the collapsibility of veins on venous pressure, including a new procedure for measuring tissue pressure. Journal of Clinical Investigation, 23, 333-341.
[18] Goel, M.S. and Diamond, S.L. (2002) Adhesion of normal erythrocytes at depressed venous shear rates to activated neutrophils, activated platelets, and fibrin polymerized from plasma. Blood, 100, 3797-3803.
[19] Michaux, G., Hewlett, L.J., Messenger, S.L., et al. (2003) Analysis of intracellular storage and regulated secretion of 3 von Willebrand disease-causing variants of von Willebrand factor. Blood, 102, 2452-2458.
[20] Prasad Chennazhy, K. and Krishnan, L.K. (2005) Effect of passage number and matrix characteristics on differentiation of endothelial cells cultured for tissue engineering. Biomaterials, 26, 5658-5667.
[21] Schwartz, E.A., Bizios, R., Medow, M.S. and Gerritsen, M.E. (1999) Exposure of human vascular endothelial cells to sustained hydrostatic pressure stimulates proliferation. Involvement of the alphaV integrins. Circulation Research, 84, 315-322.
[22] O’Grady, N.P., Alexander, M., Burns, L.A., et al. (2011) Guidelines for the prevention of intravascular catheterrelated infections. American Journal of Infection Control, 39, S1-S34.
[23] Yamakuchi, M., Kirkiles-Smith, N.C., Ferlito, M., et al. (2007) Antibody to human leukocyte antigen triggers endothelial exocytosis. Proceedings of the National Academy of Sciences USA, 104, 1301-1306.

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