Abstract
Cardiac catheterization via the transradial approach has increased in the United States over the past few years; however, wide-scale adoption still lags in comparison to many international health care systems. Transradial catheterization has a unique set of complications and risks that each operator must appreciate. Radial artery spasm and radial artery occlusion are the most common complications, while bleeding complications such as hematomas and perforations are much less frequent. Each of these issues can be managed successfully with minor changes to one’s practice. In this review of the current state of the art, the reader will develop an appreciation for the prevalence of each of the common complications as well as the less common, but potentially highly morbid, events. Throughout this evidence-based review, practical prevention strategies and specific treatment pathways are described for each issue that is covered.
1
Introduction
The transfemoral (TF) approach to coronary angiography and intervention is currently the favored access site for most operators in the United States. In 1989, Campeau reported the feasibility of coronary angiography through the transradial (TR) approach . The first TR coronary stent implantation was reported by Kiemeneij and Laarman in 1993 . The benefits of the radial approach are primarily related to a decrease in bleeding and vascular access site complications . Interestingly, in a recent randomized trial that compared TF and TR access sites, the authors noted no difference in Thrombolysis in Myocardial Infarction major bleeding between the TR and TF approach . Nonetheless, major vascular access site complications were significantly less frequent in the TR group (1.4%) compared to the TF group (3.7%) (hazard rate 0.37, confidence interval 0.27–0.52, P <.0001). Other reported advantages of the TR technique include improved patient satisfaction, decreased length of stay and an enhanced economic outlook .
Given these findings, the radial artery approach has found a strong following in Europe, Asia and Canada for several years. This has not been the case in the United States. In the United States, through 2007, the transradial approach accounted for only 1.3% of cases. Most centers used the radial approach in less than 10% of cases, with only seven centers performing radial percutaneous coronary intervention (PCI) in >40% of all cases .
Several possible explanations exist to explain this divergent approach to vascular access. In order to master a new technique, a learning period is required — the transradial approach is no different . Every procedure has a unique set of complications and challenges that require specific preventative measures and management strategies. Knowledge of the complications encountered during transradial catheterization and the most effective means to avoid them is essential in starting a successful radial program ( Table 1 ). This paper will review the common complications encountered in performing transradial catheterization, prevention strategies and methods of treatment.
| Common complications |
| Radial artery spasm |
| Radial artery occlusion |
| Rare complications |
| Arterial perforation/dissection |
| Arterial eversion |
| Compartment syndrome |
| Catheter entrapment |
| Cardiovocal syndrome |
| Atheroembolism/thromboembolism |
2
Radial artery spasm
Radial artery spasm (RAS) is a well-known obstacle associated with this approach and continues to be a source of frustration for operators as they transition to radial access. The incidence of RAS decreases rapidly with experience perhaps as a result of improved access technique and minimizing catheter manipulation . Despite this, it remains the most common cause of procedural failure . The reported incidence of RAS in the literature has varied from 5% to as high as 30% in some series , with most recent literature reporting spasm in 10% of cases. Predictors of spasm include younger age, female gender, diabetes, smaller wrist circumference and lower body weight .
The tendency for the radial artery to spasm has long been appreciated. From a histological perspective, the radial artery is classified as a Type III artery (limb) that is more prone to spasm as compared to Type I (somatic) or Type II (splanchnic) arteries . In vitro studies have demonstrated that the radial artery is an α-1 adrenoreceptor-dominant artery. Unlike other arterial conduits, the radial artery also has functional postjunctional α-2 adrenoreceptors that may explain its exaggerated vasospastic response to circulating catecholamines . Radial artery spasm refers to friction between the artery and wires or guide catheters accompanied by a subjective feeling of pain. Pain from RAS increases vasomotor tone resulting in further spasm. Kiemeneij et al. demonstrated objective evidence of RAS by direct force measurement using mechanical pullback devices during sheath removal . Patients with clinical RAS had a measured maximal pullback force (MPF) of >1.0 kg. No patient with an MPF <1.0 kg experienced pain. This device was then used to monitor the effect of various antispasmodic drug combinations, frequently referred to as “cocktails,” as well as the addition of a hydrophilic coating to the sheath. All of these interventions decreased MPF as well as clinical RAS. In current practice, careful puncture technique, antispasmodic “cocktails” and hydrophilic-coated sheaths are the mainstays of RAS prevention .
2.1
RAS prevention: antispasmodic medications
A strategy of prevention rather than treatment of RAS will improve procedural success rates and decrease procedure duration . Intraarterial (IA) administration of antispasmodic medications has been shown to decrease the incidence of RAS . Calcium channel blockers, nitrates, local anesthetics (e.g., lidocaine) and α-antagonists are the most common medications used for this purpose ( Table 2 ). These medications or mixture of medications (“cocktail”) are usually administered via the access sheath into the radial artery after sheath insertion and with catheter exchanges.
| Study medications with dose a (rates of spasm) | Result | Reference | |
|---|---|---|---|
| Verapamil (2.5 mg) (13.2%) | Phentolamine (2.5 mg) (23.2%) | Verapamil superior b ( P =.004) | Ruiz-Salmeron, CCI 2005;66:192–198 |
| Nicorandil (4 mg) (50.7%) | Verapamil (0.1 mg)+NTG (200 μg) (52%) | No difference c ( P >.05) | Kim, Int J Cardiol 2007;120:325–330 |
| Verapamil (5 mg)+NTG (200 μg) (8%) | Placebo (22%) | Verapamil+NTG superior d ( P =.029) | Kiemeneij, CCI 2003;58:281–284 |
| NTG (100 μg)+verapamil (1.25 mg) (3.8%) | NTG (100 μg) (4.4%) | • No difference e ( P =.804) • Both superior to placebo ( P =.001, P =.003) | Chen, Cardiology 2006;105:43–47 |
| NTG (100 μg)+sodium nitroprusside (100 μg) (9.5%) | NTG (100 μg) (12.2%) | No difference b ( P =.597) | Coppola, J Invasive Cardiol 2006;4155–8 |
| NTG (100 μg)+sodium nitroprusside (100 μg) (9.5%) | Sodium nitroprusside (100 μg) (13.4%) | No difference b ( P =.597) | Coppola, J Invasive Cardiol 2006;4155–8 |
a All routes of administration are IA. Rates of spasm in parentheses.
b Spasm determined by clinical assessment.
c Spasm determined by angiographic assessment.
Kiemeneij et al. showed a 14% reduction in RAS with the use of a “cocktail” containing verapamil 500 μg and nitroglycerin 200 μg . Coppola et al. found that addition of sodium nitroprusside, a direct nitric oxide donor, to nitroglycerin resulted in no further reduction in RAS and that sodium nitroprusside and nitroglycerin were equally effective . Verapamil, a nondihydropyridine calcium channel blocker, has negative inotropic effects, and therefore, some have called for caution when using it in patients with left ventricular dysfunction . Given these concerns, Chen et al. evaluated three antispasmodic strategies: nitroglycerin and verapamil, nitroglycerin alone and placebo. All patients received unfractionated heparin (UFH). Approximately 4% of patients in the nitroglycerin group developed RAS, similar to the incidence of RAS among the patients who received verapamil and nitroglycerin (3.8%). Both treatment strategies led to a lower incidence of RAS compared to the control group (20%) .
Nicorandil is an effective vasodilator of peripheral arteries through its potassium channel-activating effects as well as dilatation of systemic veins and epicardial coronary arteries through its nitrate moiety. Nicorandil 4 mg IA was compared to verapamil by Kim et al. and found to be equally effective in preventing RAS ; however, nicorandil is currently unavailable in the United States. Ruiz-Salmeron et al. found that phentolamine, a potent α-antagonist, was not as effective as verapamil in preventing RAS (23.2% in the phentolamine group vs. 13.2% in the verapamil group, P =.004) . While there is no consensus on the exact regimen or dose ( Table 2 ), the routine use of an antispasmodic “cocktail” containing a calcium channel blocker with or without a nitrate is an effective strategy in decreasing the occurrence of RAS.
2.2
RAS prevention: sheath selection
Hydrophilic-coated sheaths have been shown in multiple studies to decrease the incidence of RAS and improve patient comfort during sheath insertion and removal by lowering the friction between the sheath and radial artery wall . Kiemeneij et al. randomized patients to hydrophilic-coated or uncoated sheaths. Patient discomfort was significantly lower and sheath withdrawal required less force in the hydrophilic-coated sheath group, although there was no difference in RAS between the groups. Potential explanations for these observations may have also included operator experience and the use of antispasmodic cocktail during sheath insertion .
Rathore et al. demonstrated significantly less RAS among patients who received a hydrophilic-coated sheath compared to patients with uncoated sheaths (19% vs. 40%, P <.001) . In this study, routine use of a vasodilator “cocktail” was avoided. In addition, the impact of sheath length on the incidence of RAS was studied. It has been suggested that a longer sheath may protect the entire length of the radial artery from catheter and wire manipulation at the time of equipment exchanges . To the contrary, others have reported that, should spasm develop, a longer sheath would prove more difficult to remove and in extreme cases may lead to avulsion of the radial artery . Rathore et al. found no reduction in spasm with long (23 cm) vs. short (13 cm) arterial sheaths. There was a higher rate of radial artery occlusion (RAO) at the 4- to 6-month follow-up visit in the long- vs. the short-sheath group (8.3% vs. 5.3%, respectively, P =.042) . A complication that seems to be unique to the use of hydrophilic-coated sheaths is the development of a local allergic/inflammatory reaction to the hydrophilic coating. While initially seen only with one particular sheath manufactured by Cook Medical (Bloomington, IN, USA), there have been recent reports of the reaction associated with the newer Terumo Glidesheath (Terumo Interventional Systems, Somerset, NJ, USA) .
Prevention of RAS is multifactorial and incorporates many difficult-to-quantify components including patient education, preprocedure sedation and appropriate analgesia. By implementing many of the concepts described in this section, operators can keep rates of clinically significant RAS to a minimum.
2.3
RAS: treatment
If clinically severe spasm does occur, it can often be treated successfully with repeated doses of IA vasodilators, local anesthetics, increased analgesia and sedation, and patience. In extreme cases, operators have successfully employed an axillary nerve block, deep sedation with propofol or even general anesthesia to allow sheath removal . Care must be taken not to forcibly remove equipment should resistance occur as this can cause transection or eversion endarterectomy of the adherent section of the radial artery .
2
Radial artery spasm
Radial artery spasm (RAS) is a well-known obstacle associated with this approach and continues to be a source of frustration for operators as they transition to radial access. The incidence of RAS decreases rapidly with experience perhaps as a result of improved access technique and minimizing catheter manipulation . Despite this, it remains the most common cause of procedural failure . The reported incidence of RAS in the literature has varied from 5% to as high as 30% in some series , with most recent literature reporting spasm in 10% of cases. Predictors of spasm include younger age, female gender, diabetes, smaller wrist circumference and lower body weight .
The tendency for the radial artery to spasm has long been appreciated. From a histological perspective, the radial artery is classified as a Type III artery (limb) that is more prone to spasm as compared to Type I (somatic) or Type II (splanchnic) arteries . In vitro studies have demonstrated that the radial artery is an α-1 adrenoreceptor-dominant artery. Unlike other arterial conduits, the radial artery also has functional postjunctional α-2 adrenoreceptors that may explain its exaggerated vasospastic response to circulating catecholamines . Radial artery spasm refers to friction between the artery and wires or guide catheters accompanied by a subjective feeling of pain. Pain from RAS increases vasomotor tone resulting in further spasm. Kiemeneij et al. demonstrated objective evidence of RAS by direct force measurement using mechanical pullback devices during sheath removal . Patients with clinical RAS had a measured maximal pullback force (MPF) of >1.0 kg. No patient with an MPF <1.0 kg experienced pain. This device was then used to monitor the effect of various antispasmodic drug combinations, frequently referred to as “cocktails,” as well as the addition of a hydrophilic coating to the sheath. All of these interventions decreased MPF as well as clinical RAS. In current practice, careful puncture technique, antispasmodic “cocktails” and hydrophilic-coated sheaths are the mainstays of RAS prevention .
2.1
RAS prevention: antispasmodic medications
A strategy of prevention rather than treatment of RAS will improve procedural success rates and decrease procedure duration . Intraarterial (IA) administration of antispasmodic medications has been shown to decrease the incidence of RAS . Calcium channel blockers, nitrates, local anesthetics (e.g., lidocaine) and α-antagonists are the most common medications used for this purpose ( Table 2 ). These medications or mixture of medications (“cocktail”) are usually administered via the access sheath into the radial artery after sheath insertion and with catheter exchanges.
| Study medications with dose a (rates of spasm) | Result | Reference | |
|---|---|---|---|
| Verapamil (2.5 mg) (13.2%) | Phentolamine (2.5 mg) (23.2%) | Verapamil superior b ( P =.004) | Ruiz-Salmeron, CCI 2005;66:192–198 |
| Nicorandil (4 mg) (50.7%) | Verapamil (0.1 mg)+NTG (200 μg) (52%) | No difference c ( P >.05) | Kim, Int J Cardiol 2007;120:325–330 |
| Verapamil (5 mg)+NTG (200 μg) (8%) | Placebo (22%) | Verapamil+NTG superior d ( P =.029) | Kiemeneij, CCI 2003;58:281–284 |
| NTG (100 μg)+verapamil (1.25 mg) (3.8%) | NTG (100 μg) (4.4%) | • No difference e ( P =.804) • Both superior to placebo ( P =.001, P =.003) | Chen, Cardiology 2006;105:43–47 |
| NTG (100 μg)+sodium nitroprusside (100 μg) (9.5%) | NTG (100 μg) (12.2%) | No difference b ( P =.597) | Coppola, J Invasive Cardiol 2006;4155–8 |
| NTG (100 μg)+sodium nitroprusside (100 μg) (9.5%) | Sodium nitroprusside (100 μg) (13.4%) | No difference b ( P =.597) | Coppola, J Invasive Cardiol 2006;4155–8 |
a All routes of administration are IA. Rates of spasm in parentheses.
b Spasm determined by clinical assessment.
c Spasm determined by angiographic assessment.
Kiemeneij et al. showed a 14% reduction in RAS with the use of a “cocktail” containing verapamil 500 μg and nitroglycerin 200 μg . Coppola et al. found that addition of sodium nitroprusside, a direct nitric oxide donor, to nitroglycerin resulted in no further reduction in RAS and that sodium nitroprusside and nitroglycerin were equally effective . Verapamil, a nondihydropyridine calcium channel blocker, has negative inotropic effects, and therefore, some have called for caution when using it in patients with left ventricular dysfunction . Given these concerns, Chen et al. evaluated three antispasmodic strategies: nitroglycerin and verapamil, nitroglycerin alone and placebo. All patients received unfractionated heparin (UFH). Approximately 4% of patients in the nitroglycerin group developed RAS, similar to the incidence of RAS among the patients who received verapamil and nitroglycerin (3.8%). Both treatment strategies led to a lower incidence of RAS compared to the control group (20%) .
Nicorandil is an effective vasodilator of peripheral arteries through its potassium channel-activating effects as well as dilatation of systemic veins and epicardial coronary arteries through its nitrate moiety. Nicorandil 4 mg IA was compared to verapamil by Kim et al. and found to be equally effective in preventing RAS ; however, nicorandil is currently unavailable in the United States. Ruiz-Salmeron et al. found that phentolamine, a potent α-antagonist, was not as effective as verapamil in preventing RAS (23.2% in the phentolamine group vs. 13.2% in the verapamil group, P =.004) . While there is no consensus on the exact regimen or dose ( Table 2 ), the routine use of an antispasmodic “cocktail” containing a calcium channel blocker with or without a nitrate is an effective strategy in decreasing the occurrence of RAS.
2.2
RAS prevention: sheath selection
Hydrophilic-coated sheaths have been shown in multiple studies to decrease the incidence of RAS and improve patient comfort during sheath insertion and removal by lowering the friction between the sheath and radial artery wall . Kiemeneij et al. randomized patients to hydrophilic-coated or uncoated sheaths. Patient discomfort was significantly lower and sheath withdrawal required less force in the hydrophilic-coated sheath group, although there was no difference in RAS between the groups. Potential explanations for these observations may have also included operator experience and the use of antispasmodic cocktail during sheath insertion .
Rathore et al. demonstrated significantly less RAS among patients who received a hydrophilic-coated sheath compared to patients with uncoated sheaths (19% vs. 40%, P <.001) . In this study, routine use of a vasodilator “cocktail” was avoided. In addition, the impact of sheath length on the incidence of RAS was studied. It has been suggested that a longer sheath may protect the entire length of the radial artery from catheter and wire manipulation at the time of equipment exchanges . To the contrary, others have reported that, should spasm develop, a longer sheath would prove more difficult to remove and in extreme cases may lead to avulsion of the radial artery . Rathore et al. found no reduction in spasm with long (23 cm) vs. short (13 cm) arterial sheaths. There was a higher rate of radial artery occlusion (RAO) at the 4- to 6-month follow-up visit in the long- vs. the short-sheath group (8.3% vs. 5.3%, respectively, P =.042) . A complication that seems to be unique to the use of hydrophilic-coated sheaths is the development of a local allergic/inflammatory reaction to the hydrophilic coating. While initially seen only with one particular sheath manufactured by Cook Medical (Bloomington, IN, USA), there have been recent reports of the reaction associated with the newer Terumo Glidesheath (Terumo Interventional Systems, Somerset, NJ, USA) .
Prevention of RAS is multifactorial and incorporates many difficult-to-quantify components including patient education, preprocedure sedation and appropriate analgesia. By implementing many of the concepts described in this section, operators can keep rates of clinically significant RAS to a minimum.
2.3
RAS: treatment
If clinically severe spasm does occur, it can often be treated successfully with repeated doses of IA vasodilators, local anesthetics, increased analgesia and sedation, and patience. In extreme cases, operators have successfully employed an axillary nerve block, deep sedation with propofol or even general anesthesia to allow sheath removal . Care must be taken not to forcibly remove equipment should resistance occur as this can cause transection or eversion endarterectomy of the adherent section of the radial artery .
3
Radial artery occlusion
Radial artery occlusion (RAO) is a well-recognized complication of radial artery cannulation. In certain clinical contexts, such as prolonged hemodynamic monitoring in the perioperative period, rates of RAO have been reported to be as high as 30%–40% . The incidence of RAO after transradial catheterization, however, has been significantly lower, with most series reporting RAO in 3%–10% of procedures . Spontaneous recanalization of the radial artery occurs frequently, and consequently, the prevalence of persistent RAO is much lower . Radial artery occlusion can be documented by an abnormal Barbeau’s test , visible obstruction on two-dimensional ultrasound or absence of Doppler flow signal distal to the puncture site . The presence of a radial artery pulse does not rule out RAO due to the presence of collateral circulation through the palmar arches ( Fig. 1 ).
A recent consensus statement recommends routine screening of patients for the presence of dual palmar arch circulation using Barbeau’s test, also referred to as the modified Allen’s test , with consideration given to alternative access strategies in patients who have an abnormal screening study . No studies exist demonstrating a reduction in RAO with testing for dual palmar arch circulation and this matter remains controversial among transradial operators. However, patients with an abnormal modified Allen’s test demonstrate early evidence of hand ischemia with RAO compared to patients with a normal study .
Radial artery occlusion is usually clinically quiescent, although a recent case report described significant hand ischemia in a patient following a transradial intervention . The presence of RAO, however, makes repeat ipsilateral radial access difficult . Predictors of RAO include low body weight, advanced age, female gender, degree of systemic anticoagulation, the hemostasis process as well as a low radial artery diameter to sheath size ratio ( Table 3 ).
