This chapter is vaguely relevant to Section G7(iii) of the 2017 CICM Primary Syllabus, which asks the exam candidate to "describe the invasive and non-invasive measurement of blood pressure, including limitations and potential sources of error". At a stretch, limitations and potential sources of error could be extended to include the possible complications of insertion. At this stage, no specific questions on this topic have ever come up in the exams, but it is a subject matter sufficiently ubiquitous to merit at least a brief discussion.
The best resource for this topic is the widely quoted clinical review by Scheer et al (2002). The review covered 20,000 instances of arterial line insertion and computed the risk profile by site. The risk of major complications was roughly 1 % for all sites.
At all sites, some complications are common:
Dorsalis pedis artery
Thrombotic occlusion is by far the most common complication at all sites. The radial artery and the dorsalis pedis artery as most prone to thrombotic complications. Scheer et al (2002) found that the rate of thrombosis and temporary occlusion was as high as 19.7% with radial arterial lines, as compared to 1.45% with femoral lines. Thrombosis can also occur following the removal of the line. The biggest risk factor for this seems to be the relationship of the arterial line diameter to the diameter of the lumen, i.e. the more of the lumen the catheter takes up the more likely a thrombus is to form. It takes up to 75 days to recanalize.
Lesser risk factors are being a female (with narrower arteries), having low cardiac output, having multiple attempts at cannulation and having the catheter stay in for longer than 72 hours. A hematoma at the site of puncture is also a risk factor for occlusion.
The vessel recanalises after approximately 3 weeks. This temporary occlusion is usually without serious sequelae, owing to the generous collateral circulation at these sites; less than 1% of cases require surgical intervention. Most patients who develop clinically significant ischemia have some associated contributing cause, such as high-dose vasopressor therapy or severe peripheral vascular disease. There used to be a tendency among intensivists to use a heparinised flush solution, but this is no longer recommended, as it does not appear to be protective against thrombosis and is associated with a risk of heparin-induced thrombocytopenia.
If clinically significant ischaemia is observed, immediate removal of the catheter will minimise the ensuing complications. If ischamia persists following catheter removal, the following options can be explored:
If clinically significant ischaemia is detected, it should be reported to the senior medical officer with urgency, and the need for a vascular surgical consult should be discussed with the intensivist.
“Luxury of sampling” can be viewed as a complication. The convenience of access, “leave it in one more day” mentality and the intensivist’s preoccupation with numbers tends to increase the rate of iatrogenic blood loss, as the patient exsanguinates slowly through the sample port of the blood gas analyser. Generally, 2-3ml of blood is discarded for each arterial blood gas sample, and daily blood sampling for biochemistry can contribute a further 20-30ml. Smoller et al (1986) found that the total blood lost to phlebotomy in non-ICU patients was approximately 175ml over the whole period of their hospital stay. However in the ICU this increased to 300ml for patients without arterial lines. When the patients had an arterial line, this blood loss rate increased to over 900 ml, with implications for their transfusion requirements.
The abovementioned Scheer et al (2002) study reports that the risk of arterial line related infection increases after 96 hours, but is still overall quite low, with arterial line-related sepsis found in 0.13% of cases. This risk is about half of the risk of central line related infection - approximately 3.4 per every 1000 arterial catheter days, versus 5.9 per every 1000 CVC-days (Safdar et al, 2013).
In any case, the widely held belief is that this risk of infection can be managed by changing the disposable transducer and fluid lines, instead of the catheter itself. We don't know whether this decreases the risk of infection. However, there is evidence that doing it any more frequently than every 96 hours does nothing to reduce the risk of infection (this is extrapolated from data about IV giving sets in general)
Cerebral embolisation is a known complication of flushing the arterial line. Retrograde passage of small bubbles of gas into the arterial circulation is possible, considering that the pressure transducer is coupled to a bag with 300mmHg of pressure (i.e. enough to defeat systemic arterial pressure).
Risk factors for clinically significant cerebral gas embolism include the following:
For Chang et al (1988), a case of a woman who became braindead after such an event prompted an exploration by means of a primate model. Macques had their radial arteries cannulated and were injected with radioactive xenon (133Xe). With volumes in the range of 2.5-5ml, gas was seen in the brain. The study has limitations: heavy inert xenon is a poor surrogate for air, and macaques are much smaller than humans and therefore have a smaller arterial volume (i.e. the gas would have further top travel in a human). Moreover, the volume of gas in that study is quite substantial. Given that according to manufacturer brochures the incompressible polyurethane tubing has an internal diameter of 1.8mm, one would have to fill about 100cm of tubing with air to get a gas volume of 2.5ml. In short, your little bubbles in the tubing set are not likely to cause a retrograde embolism (though they are certainly not very good for the hand).