Take care from start to finish: Avoiding radial artery occlusion

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Root cause analysis of radial occlusion points to vessel trauma. An ultrasound study by Costa et al demonstrated that in the setting of a 6Fr vascular sheath placed into the radial artery, 100% of the arteries manifested traumatic injury. 1

Dissection, haematoma, and pseudoaneurysm were seen in the majority of patients, yet only 4% showed intraluminal thrombus in these heparinised patients. This finding suggests that traumatic vessel injury rather than primary thrombus is the underlying problem. In this commentary, Ian C Gilchrist looks at the causes of radial occlusion and how to avoid the complication.

The advent of dorsal radial access and the observation that radial artery occlusion tends to be limited to the dorsal branch rather than extension into the radial proper highlights the dominant role the vessel wall injury has in initiating the radial artery occlusion process.2

How can radial artery damage be limited? Use the smallest sheath needed to do the job! As one moves down a French size, each jump reduces the baseline radial occlusion rate by about 50%. Therefore if one has a 5% occlusion rate at 6Fr, using 5Fr will result in a 2.5% occlusion rate—and 4Fr sheath would result in a 1.25% rate. The number of attempts at access (how many needle sticks) is a measure of trauma and minimising the need for multiple needle sticks also results in less radial occlusion. Ultrasound technology and micropuncture needles all curtail trauma at the time of access. Finally, the use of hydrophilic sheath technology that facilitates a smooth entry into the radial artery probably adds to reducing trauma.

Sheaths in small arteries, such as the radial, usually produce radial spasm that further enhances blood stasis and thrombosis. Antispasm regimens, also referred to as “cocktails”, and analgesia to reduce sympathetic tone may counter some of the spasm. The most important addition is heparin, or its equivalent, at a therapeutic dose on the order of 5,000U. Full dose heparin has been shown superior to lesser regimens or no anticoagulation. Oral anticoagulants have not been shown to substitute for this protective effect afforded by systemic anticoagulation. Heparin likely controls thrombosis both early on around the sheath before its removal and then along the acutely injured artery and the entry site during haemostasis.

At the conclusion of the case, haemostasis techniques affect the potential for ultimate radial artery occlusion. Zip bands were quick, but their mechanism of action probably resulted from thrombus-driven occlusion. Pancholy et al coined the term “patent haemostasis” to describe an approach to haemostasis that maintains luminal flow without extra-vascular extravasation.3 It is a “Goldilocks” approach of “not too tight, not to lose, but just enough” pressure on the radial entry site to maintain flow without resulting bleeding.

What can be done if, despite all the best efforts, there appears to be radial artery occlusion after haemostasis? Bernat et al have demonstrated that application of occlusive pressure to the ipsilateral ulnar will often result in rapid resolution of an acute radial occlusion.4 While mechanical disruption of thrombus may be possible, this appears to have the risk of distal embolisation into the finger tips that is not a welcome complication.

Putting this all together, radial artery occlusion can be and should be reduced to less than 1%. Using the best sized sheath for the procedure, careful cannulation with a micropuncture needle under ultrasound guidance, pharmacologic control of thrombus formation, patent haemostasis at the conclusion of the procedure, and ulnar compression for bailout in the case of acute radial occlusion, the net loss of radial arteries can be minimized to the point that most will remain available for use in the future. Radial artery catheterisation is the way to proceed for procedures suitable for the vessel’s size. It is a low-risk access point, but care is needed to maximise its long-term use.

References

  1. Costa et al. Circ Cardiovasc Interv 2016; 9 (2): e003129.
  2. Kiemeneij. EuroIntervention 2017; 13(7): 851–57.
  3. Pancholy et al. Catheter Cardiovasc Interv 2008; 72(3): 335–40.
  4. Bernat et al. Am J Cardiol 2011; 107(11): 1698–701.

Ian C Gilchrist is at Pennsylvania State University, College of Medicine, Heart & Vascular Institute, M.S. Hershey Medical Center, Hershey, USA. He spoke about this topic at the CRT 2018 (3–6 March, Washington, DC, USA)

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