CVC is the initial or long-term vascular access for most patients with MHD. CVS or occlusion secondary to catheter insertion causes permanent damage to blood vessels and many serious problems related to the obstruction of central venous return. Moreover, it accelerates vascular access resource depletion, seriously affecting the quality of dialysis and long-term prognosis20.
Unfortunately, the exact pathogenesis of CVC-related CVS remains undetermined. The possible pathogenic mechanisms proposed so far include mechanical injury during catheter insertion, turbulence of blood flow in the location of the intravascular catheter, coagulation cascade and inflammation caused by prolonged catheter indwelling19,21. In addition, Alian et al. suggested that CVS significantly correlated with the retention time of catheters with a Dacron cuff22. Forauer et al. conducted a pathological study of the vascular intima of patients with central venous catheterization and found that local damage to the vascular intima, including intimal denudation and adhesion thrombus, was observed within 14 days after catheter insertion. Meanwhile, long-term catheterization (> 90 days) induced thickening of the venous intima, and thrombus, collagen and endothelial cells in different stages can be found in the area where the catheter contacts the venous intima23. These phenomena suggest that CVC-induced CVS is a chronic and progressive pathology that cannot be explained simply by puncture injury. Based on the results of studies on urethral friction damage caused by urinary catheters, friction injury caused by cardiovascular catheters on the blood vessel, tests on surface lubrication, characteristics of various movements, and long-term indwelling of CVCs for dialysis in the central vein, CVCs for HD will also cause mechanical friction damage to the inner membrane of the central vein24,25,26. For the first time, Leblanc et al. proposed that the stiffness of the catheter might be relevant to the initiation or progression of the vascular intima wear or catheter-induced irritation, leading to chronic vascular endothelial injury27. An earlier study also suggested that relatively soft silicone catheters were associated with lower incidence of thrombosis than stiffer polyethylene dialysis catheters28, which also indirectly confirmed that different stiffnesses of catheters had different effects on vascular endothelial injury. Some studies have also reported delayed vascular injury after catheterization, and progressive vascular injury in these cases can be present up to 35 days after catheterization29. The above studies have directly or indirectly indicated that CVC indwelling is related to chronic mechanical friction injury of the vascular intima.
When chronic mechanical friction trauma occurs, local inflammatory responses and oxidative stress in damaged blood vessel walls are triggered, resulting in the release of peroxidase and activation of the thrombin cascade, and promoting endothelial hyperplasia, central vein thrombosis, vascular stenosis or occlusion and other serious complications19. Studies have revealed that approximately 20 to 40% of patients with CVCs on MHD were diagnosed with CVS30. Meanwhile, some patients without any clinical symptoms can only be accidentally found to have CVS related to the location of the original catheter during imaging examination months or years after CVC removal. This indicated that the real incidence of CVC-induced CVS may be higher than the existing estimated data. Lin et al. conducted in vitro tests, mimicking the reciprocating sliding motion between a blood vessel and a catheter, and indicated that decreasing catheter stiffness and endothelial glycocalyx layer (EGL) degradation were the strongest factors that increased the coefficient of friction at the aorta–catheter interface31. EGL damage is related to inflammation, oxidative stress, and other vascular damage factors.
Thus, we speculate that CVC indwelling may cause chronic mechanical friction injury to the vascular intima, which may be a crucial initiating or inducing factor for subsequent inflammation and oxidative stress in damaged blood vessels, and central venous thrombosis, stenosis, or occlusion.
To explore the relationship between the surface roughness of the catheter and vascular intima trauma, material surface observation and in vitro friction experiments were conducted. By combining the characteristics of the catheter displacement in vivo observed through catheter angiography and clinical experience, we considered that the friction between the catheter and the vascular intima is mainly linear, the contact loading force between the two surfaces is small, and the friction speed is relatively slow. Owing to the presence of blood in the vein, a mixed friction mode exists between the catheter and the vascular intima. According to our previous experience, we immersed blood vessels in 0.9% saline solution in the in vitro experiments to simulate the frictional environment between the catheter and the inner membrane in vivo as much as possible under CVC indwelling.
The results of SEM and 3D white-light interferometry showed that the surface microstructure of the catheter was not smooth, particularly in some angles or sections, such as the tip of catheter where the roughness was relatively high. The morphology and roughness of the vascular intima also changed before and after the friction in vitro experiment, which can indicate that the catheter caused mechanical friction injury to the vascular intima during linear friction. Statistical analysis of the experiment confirmed that the surface roughness of the catheter positively correlated with the friction coefficient when it contacted the vascular intima, which was consistent with our initial hypothesis and results of various vascular injuries caused by indwelling catheters, as observed in previous studies. The catheter was originally designed to provide adequate blood flow while limiting recirculation rates32. Previous studies suggested that the macroscopic morphology of catheter tip may cause vascular damage13. Our study reveals, for the first time, that differences in the microscopic morphology of the roughness of catheters also have an impact on central venous endothelial damage. Therefore, when the catheter is placed in the central vein for a long time, the HD catheter with high surface roughness may cause relatively serious and continuous mechanical friction damage to the vascular intima (Fig. 6) and may be more likely to induce CVS and thrombosis.
Simulation of the difference in friction damage caused by catheters of different roughness to the vascular intima.
At present, little attention has been paid to chronic mechanical friction trauma induced by catheters for HD on the central veins, including the superior vena cava, and no specific studies have been conducted. In addition, quantitative evaluation of the surface roughness of CVCs is lacking worldwide, and no clear standard and management of catheter surface roughness has been established. This study suggests that friction injury from rough catheter surfaces is a potential inducing factor for CVS and thromboembolism in patients with long-term indwelling CVC, which is worthy of attention. This result may serve as an entry point to reduce CVC-related complications and improve patient prognosis. In the future, more in vitro and clinical studies are needed to clarify the mechanism and downstream effects of friction damage between catheters and central veins, formulate clear parameters and management norms for catheter surface roughness, and promote the development of catheter surface lubrication technology. Essentially, not only CVCs are used for dialysis; peripherally inserted central catheters (PICCs) also have similar problems. They migrate with respiration, bloodstream flow dynamics, postural rotation and neck movements, injuring the blood vessel wall by rubbing33; thus, this experimental outcome may extend to PICCs.
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- Source: https://www.nature.com/articles/s41598-024-56485-5