Access Site Complications



An understanding of access site complications is essential for the invasive cardiologist. Access site complications are associated with increased morbidity and all-cause mortality, and cessation of evidence-based therapies. While absolute rates of major access site complications are low, the large volume of yearly endovascular interventions means that many patients are affected by these complications despite best practices. In this chapter we review the most common complications that can occur in the catheterization laboratory by access site and outline evidence- and experience-based measures and techniques for the prevention and management of these events.

29.1 Introduction

Over one million diagnostic coronary angiograms and 350,000 percutaneous interventions are performed in the USA annually [1]. Procedural success is contingent on obtaining uncomplicated vascular access, which demands employment of consistent and meticulous cannulation and closure techniques. While absolute rates of access site complications are low (vascular complications <1%, bleeding 1.5–3.1% [2, 3]) the high volume of procedures means that a significant number of patients suffer these complications despite the operator’s best intentions. Furthermore, these complications can lead to cessation of evidence-based therapies and are associated with significant morbidity and increased all-cause mortality [3, 4]. This chapter outlines standards for optimal techniques and evidence-based strategies used in contemporary practice to minimize access site complications and optimize the safety and success of percutaneous procedures. It also provides the invasive cardiologist with an overview of both common and uncommon complications related to procedural access and their respective management.

29.2 Femoral Access Complications

Femoral arterial puncture remains a mainstay of cardiac intervention. While the use of transradial access is on the rise [5, 6], femoral access for «bailout»—as well as its requirement for complex coronary, peripheral, and structural interventions—remains a critical skill for the invasive cardiologist. A firm understanding of optimal technique for transfemoral access and its inherent possible complications is needed.

29.2.1 Bleeding

Bleeding is the most common complication of femoral arterial access. Overall, the rates of major bleeding remain relatively low, with significant bleeding following percutaneous coronary intervention (PCI) estimated at 3.1% [3]. In this section we first discuss definitions and risk factors for bleeding complications related to the access site, followed by the most common presentations of bleeding to be encountered by invasive cardiologists, and conclude by reviewing strategies that clinicians can pursue to mitigate bleeding risk.

Definitions of Bleeding

Access site bleeding complications can vary widely in regard to severity and clinical impact, from a small hematoma causing discomfort to life-threatening large-volume bleeding. Bleeding complications have been associated with an increased risk of adverse patient outcomes, including myocardial infarction, stroke, stent thrombosis, and death in patients with ACS and those undergoing PCI [7]. Various definitions of bleeding severity have emerged in the study of bleeding after PCI, including the commonly referenced TIMI and GUSTO bleeding definitions [8, 9]. However, the heterogeneity of these definitions of bleeding has limited the ability of clinicians to accurately synthesize and compare the broad data available on bleeding complications. In an effort to standardize the definition of bleeding, the Bleeding Academic Research Consortium (BARC) synthesized prior classifications into a novel «universal definition» aimed to be broadly applicable to clinical practice and scientific evaluation alike, to effectively communicate hierarchical severity of bleeding, and to differentiate between coronary artery bypass grafting (CABG)–related bleeding and non-CABG-related bleeding (◘ Table 29.1) [7]. Clinicians’ use of the BARC definitions is strongly recommended, as these definitions promote an objective and standardized method of assessing periprocedural adverse events.
Table 29.1

Bleeding Academic Research Consortium (BARC) bleeding definition




No evidence of bleeding


Bleeding that is not actionable and does not require unscheduled treatment


Any clinically overt sign of hemorrhage that requires unscheduled diagnostic studies, hospitalization, or treatment by a healthcare professionala


Clinical, laboratory, and/or imaging evidence of bleeding


3a: Any transfusion with overt bleeding, hemoglobin drop ≥3 to <5 g/dLb


3b: Hemoglobin drop ≥5 g/dL, cardiac tamponade, requiring surgical intervention for control, requiring intravenous vasoactive drugs


3c: Intracranial hemorrhage, intraocular bleed compromising vision


Coronary artery bypass graft–related bleeding. Perioperative bleeding within 48 h, reoperation after closure of sternotomy for purposes of bleeding, transfusion of ≥5 U of whole blood or packed red blood cells within 48 h, chest tube output ≥2 L within a 24 h period


Fatal bleeding

aHealthcare professional–guided treatment or percutaneous intervention to stop or treat bleeding, including temporarily or permanently discontinuing a medication or study drug

bCorrected for intercurrent transfusion in which 1 U of packed red blood cells would be expected to increase hemoglobin by 1 g/dL

Risk Factors for Bleeding

Risk of bleeding is associated with specific patient and procedural factors, only some of which can be modulated. While certain patient factors can be mitigated by appropriate case selection (i.e., consideration of noninvasive testing or medical therapy in those at highest risk of procedural complications), once the patient arrives in the cardiac catheterization laboratory the operator should be aware of the patient’s propensity for bleeding complications. Patients who experience major bleeding complications following PCI are more likely to be older, be female, have symptomatic peripheral vascular disease, have either high or low extremes of body mass indices, and have more comorbid medical conditions [10]. Other patient-related factors associated with bleeding include patient acuity, with a fourfold excess risk of bleeding for PCI in the setting of ST-elevation myocardial infarction (STEMI) as compared with elective PCI. [11]. Procedural factors such high or low arterial puncture and use of larger sheath sizes have also been associated with increased bleeding and vascular complications [12, 13].

Common Bleeding Complications

A hematoma is a blood collection in the subcutaneous tissue outside the vessel lumen, which presents as a tender subcutaneous mass at the arteriotomy site. A hematoma most commonly results in patient discomfort, bruising, and increased infection risk. However, in rare cases, a large hematoma can cause hemodynamic instability or compression of nearby structures, such as the lateral femoral cutaneous nerve and, in extreme cases, skin necrosis (Fig. 29.1).
Fig. 29.1

Femoral hematoma after percutaneous coronary intervention via transfemoral access

After sheath removal, if a developing hematoma is present, the pulse should be localized if possible, and firm and steady fingertip pressure must be applied proximal to the skin entry point to target the arteriotomy location until hemostasis is achieved. In cases where the pulse is obscured or difficult to palpate, bedside ultrasonography can be used to identify both the vessel and an associated hematoma. After identification, manual compression can be accurately applied or, in extreme cases, hemostatic pressure can be maintained with the probe itself. A hematoma developing around an indwelling sheath is suggestive of arterial laceration but may also occur in patients with high blood pressure, particularly if combined with calcified plaques at the entry point. If a hematoma is identified and hemostasis is achieved early, massaging the area with steady pressure can often reduce the hematoma size or eliminate it completely. A stable hematoma will progress to a tender mass and bruising, and will slowly resolve after 1–2 weeks. A larger hematoma may not be absorbed at the groin and may slowly descend through the upper and lower leg compartments, frequently causing pain and discomfort. In these patients, analgesia and walking exercise are recommended to improve resorption. In rare cases where manual compression is either challenging or difficult to achieve or maintain, a FemoStop device (St. Jude Medical, Inc.) can be deployed (◘ Fig. 29.2, ◘ Table 29.2). In cases of ongoing hematoma expansion despite manual pressure or hemodynamic instability, anticoagulation should be reversed and repeat angiography via contralateral femoral access should be performed to identify any possible ongoing arterial bleeding, which may require intervention. Finally, in cases of large hematomas causing compression of nearby structures, surgical evacuation may be required.
Fig. 29.2

FemoStop device (St. Jude Medical, Inc.)

Table 29.2

FemoStop indications, cautions, and deployment

Indications for use

• Uncontrolled bleeding despite manual compression

• Anticipation of a long duration of hemostasis such as with large-bore catheters, excessive anticoagulation use, recognized hematoma, use of dual antiplatelet therapy

Cautions for use

• Do not leave at systemic pressure for over 3 min, to minimize the risk of limb ischemia

• Do not leave the system in place for excessively long durations of compression, as tissue damage or thrombosis may result (i.e., use the lowest pressure for the shortest duration possible to attain hemostasis)

• For extended compression, it is recommended to allow a brief interruption of pressure at least every 3 h

• FemoStop is not intended to replace careful monitoring. The patient should not be left completely unattended

• Use Doppler to periodically confirm whether or not flow remains in the vessels. When releasing pressure, do so slowly to minimize the risk of flushing thrombotic material distally

Step 1

• Recognize ongoing bleeding and attempt to control it with manual compression while readying the FemoStop device

Step 2

• Prior to sheath removal or prior to release of manual pressure if the sheath has already been removed, place the belt under and around the patient’s hips so it is pulled equally on both sides and is directly in line with the puncture site(s)

Step 3

• Place the center of the dome superiorly and medially relative to the skin incisions to ensure that the dome is positioned over the actual arterial puncture site

• Note: To minimize the risk of arterial/venous malformation, venous hemostasis should be achieved prior to arterial hemostasis. If a venous sheath is present, to remove the venous sheath, make sure the control knob of the pump is closed and begin to inflate the dome to 20 or 30 mmHg. Remove the venous sheath

Step 4

• To remove an arterial sheath, begin to increase the pressure to 60–80 mmHg with the control knob closed. Withdraw the arterial sheath at between 60 and 80 mmHg. As soon as the arterial sheath has been removed, continue to increase the pressure to 10–20 mmHg above systolic or higher as necessary to maintain the initial hemostasis

• Note: If «HHH» is shown on the display, too much pressure has been applied. Open the control knob and decrease the pressure immediately

Step 5

• Maintain the initial hemostasis pressure for about 1–3 min. Do not leave the artery completely occluded for more than 3 min, to minimize the risk of limb ischemia. Check the pedal pulse periodically to confirm whether or not flow remains in the vessel

Step 6

• Continue the maintenance pressure according to facility guidelines specified for the type of patient, anticoagulant level, interventional procedure performed, and sheath French size used. We recommend half the systolic blood pressure in most cases. For the duration of FemoStop compression, frequent and thorough evaluation of the distal extremity is critical to minimize the chances of precipitating limb ischemia

Step 7

• Once the above duration of time has elapsed, gradually lower the pressure in steps of 10–30 mmHg, as long as hemostasis is maintained, and observe the site for 2–3 min. Continue in this fashion until the dome is completely deflated. After a few minutes of observation at zero pressure, either proceed to remove the system as described below or leave it in place at very low pressure for as long as necessary to ensure continued hemostasis

Step 8

• Carefully loosen the belt on the puncture side of the patient without totally removing it from the arch, and gently roll the dome off the site. Observe for any bleeding. If hemostasis has been achieved, the belt can be removed entirely

Retroperitoneal Hemorrhage
Retroperitoneal hemorrhage (RPH) is a rare but life-threatening complication of femoral arterial access, which is estimated to occur in 0.2–0.4% of PCI cases [2]. Anatomically, the femoral artery enters the retroperitoneal space at the level of the inguinal ligament. This entry into the retroperitoneal space can be identified angiographically by the takeoff of the inferior epigastric artery. A bleed into this space can be rapid and large volume, and can result in acute hemodynamic instability (◘ Fig. 29.3). Entry into the retroperitoneal space is typically characterized by the vessel «diving deep,» and operators should be suspicious if the femoral access appears «deeper» than expected, especially in larger patients. While an arteriotomy site below the inguinal ligament decreases the risk of RPH, it does not eliminate the risk entirely. RPH can also occur from laceration of small arterial branch vessels that track in the retroperitoneal space. Thus, it is important to maintain a high index of suspicion for RPH in an unstable patient even when there is a mid–femoral head arteriotomy location. Use of fluoroscopic landmarks can optimize the arteriotomy position to minimize the chances of arterial cannulation proximal to the inferior epigastric artery, but must be marked and noted with care in obese individuals with distorted surface anatomic landmarks (i.e., an «offset» inguinal crease; see below ► section Bleeding Reduction Strategies).
Fig. 29.3

Contrast extravasation due to a large retroperitoneal hemorrhage

If RPH is clinically suspected, treatment should start immediately with placing a large-bore venous access, crystalloid volume expansion, anticoagulant reversal and, following appropriate testing, if needed, a blood transfusion. For unfractionated heparin, protamine sulfate is administered at 1–1.5 mg per 100 units of heparin administered for full reversal of anticoagulant effects1 (◘ Table 29.3). Treatment should not be delayed for confirmation with imaging. In stable patients, an ultrasound or abdominal and pelvic computed tomography (CT) scan with contrast can confirm the diagnosis. In the hemodynamically unstable patient, a return to the catheterization laboratory for diagnostic imaging and therapeutic percutaneous intervention may be required. If the bleeding source originates from a large artery, balloon tamponade with prolonged inflation (5–10 min) can be attempted. If this fails to stop the bleeding, a covered stent can be placed (◘ Fig. 29.4). Care should be taken to not impinge on the common femoral artery, as this represents a flexion point of the lower extremity and poses a risk of stent thrombosis with subsequent limb compromise. Small-branch arterial bleeding can be treated by coil embolization, or if endovascular strategies fail, by surgical management. Fewer than 10% of RPH cases will require surgical intervention [14]. The decision to proceed to surgical intervention should be individualized based on the site of bleeding (i.e., at a bifurcation or at the common femoral artery), ability to safely intervene using endovascular means (using covered stents, coils, or vascular plugs), and the stability of the patient. If the patient is critically unstable despite adequate resuscitation and endovascular attempts at intervention, or develops signs of abdominal compartment syndrome or other signs of mechanical compression (i.e., lumbar plexus injury) that could require evacuation, then an open surgical approach is favored.
Table 29.3

Acute management of a patient with suspected retroperitoneal hemorrhage (RPH)

Suspected RPH

• Maintain aggressive manual compression if possible at suspected bleeding site

• Establish two access sites with large-bore intravenous lines. Send a laboratory sample for a type and screen

• Volume resuscitate with crystalloid fluids and blood transfusion as needed

• If there is suspicion of a vagal response contributing to the presentation, administer atropine 1 mg intravenously

• Administer vasopressors as needed during resuscitation to stabilize hemodynamics

Hemodynamically stable patient

• Perform a CT scan of the abdomen and pelvis or repeat angiography to confirm the diagnosis and localize the site of bleeding

• The decision to pursue intervention versus conservative management is dependent on the size of the bleed, the presence of ongoing bleeding, and patient stability

Hemodynamically unstable patient

• Administer reverse anticoagulation with protamine sulfate, dosed as 1.5 mg per 100 units of heparin administered over 5–10 min for full reversal (this can be administered faster, but that can result in hypotension related to the infusion)

• Perform emergent contralateral femoral angiography to localize the site of bleeding and attempt endovascular intervention

• If endovascular attempts fail, abdominal compartment syndrome or lumbar plexus injury develops, or if the patient is critically unstable, refer for emergent surgical intervention

CT = computed tomography


a Retroperitoneal hemorrhage originating from the left external iliac artery. b Treatment with covered stent placement resolves the bleed

Arterial Laceration

An arterial laceration is a tear in the artery, which can occur both at the arteriotomy site and distal to it. An arterial laceration will present as bleeding around an indwelling sheath or as a rapidly expanding hematoma. Laceration at the arteriotomy site can occur from a sheath that is oversized for the access vessel, advancement of a sheath without a dilator, or movement of the sheath or patient during the procedure. Initial management should start with exchanging the current sheath over a supportive wire (i.e., Supracore, Abbott, Inc.; or Rosen, Angiodynamics, Inc.) for a larger-diameter sheath to tamponade the torn area. Sheath exchange and upsizing does carry a risk of extending the laceration. If there is suspicion that the sheath was oversized for the vessel diameter, obtaining contralateral femoral access or left radial access for wire and balloon occlusion of the vessel may be necessary. If tamponade is achieved, anticoagulant reversal should be performed and the sheath can be removed with a standard manual compression technique once anticoagulant effects have dissipated.

Laceration away from the arteriotomy can also occur and can present as an expanding hematoma, retroperitoneal bleeding, or hemodynamic instability, depending on the location of the laceration. An errant wire position, sheath placement, or catheter tip advancement without a dilator can result in vessel laceration away from the arteriotomy site. In cases where laceration away from the arteriotomy is suspected, it is recommended to maintain the catheter or sheath position and obtain alternative access (left radial or contralateral femoral). The vessel can be wired to maintain position within the true lumen, maintaining the catheter or sheath in position to help guide vessel wiring and potentially to limit ongoing bleeding. Reversal of anticoagulation should be performed while ensuring adequate volume resuscitation. Percutaneous options for repair depend on the location of the lesion. Balloon tamponade of the vessel (inflating the balloon as the sheath or catheter are withdrawn) can stabilize the bleeding while consultation with either a peripheral vascular interventionalist or a vascular surgeon is obtained to determine the optimal therapy (i.e., covered stent placement, coiling of vessel side branches, or surgical repair).

Bleeding Reduction Strategies

Reducing bleeding complications requires careful attention to patient selection, cannulation technique, procedural anticoagulation strategy, and size of equipment used. First, the operator is the ultimate arbiter of who should undergo the risk of invasive angiography and intervention. The operator should consider the balance between risk and benefit for each patient before the procedure begins. Many patient characteristics are nonmodifiable; however, a preprocedural assessment of overall bleeding and complication risk can help to determine this balance. Prior to each case an operator should consider the risks versus benefits to determine if an invasive approach is warranted and, if so, whether further optimization of certain factors can modify the patient risk prior to the procedure. For example, in elective cases, if platelet abnormalities and coagulopathy are present, these should be optimized prior to catheterization. Finally, a preprocedural assessment of patient bleeding risk can inform an operator’s access site, choosing a transradial approach when feasible, and other bleeding avoidance strategies. Unfortunately, Marso et al. demonstrated a risk–treatment paradox in patients undergoing PCI in the USA, where despite the association of lower bleeding rates with bleeding avoidance strategies of bivalirudin and vascular closure device use, patients at highest risk of bleeding were least likely to receive these therapies as compared with those at lower risk [15]. These findings suggest that an opportunity remains to further target the employment of evidence-based bleeding avoidance strategies in high-risk patients, and clinicians should be aware of potential biases in their use of such techniques.

Once an operator decides that an invasive strategy is warranted, optimizing the access technique is the first place wherein the bleeding risk can be mitigated. When obtaining femoral access, the optimal arterial cannulation site is at the level of the central third of the femoral head. This location is distal to where the femoral artery exits the retroperitoneal space at the level of the inguinal ligament and is proximal to the bifurcation of the common femoral artery into the superior femoris and profunda arteries in the majority of patients. The mid–femoral head provides an anatomic «anvil» for compression of the artery when applying manual pressure for hemostasis. Cannulation above the inguinal ligament can predispose the patient to bleeding into the retroperitoneal space, while arteriotomy at or below the bifurcation can lead to arteriovenous complications, make hemostasis more difficult, and potentially compromise blood flow to the lower extremity.

Optimal arteriotomy location can be guided by a combination of anatomic, fluoroscopic, and ultrasound techniques. A routine technique is to identify the upper and lower border of the femoral head via fluoroscopy with a radiodense object on the field as a reference prior to skin puncture. In obese patients with a longer distance from the skin surface to the anterior wall of the femoral artery, we recommend marking the femoral head borders on the drape rather than the skin itself with a marking pen, as compression of the subcutaneous tissue can distort any markings made on the skin surface. Additional guidance with fluoroscopy during needle insertion can aid in achieving a mid–femoral head arteriotomy site.

Another useful technique is the use of two-dimensional ultrasound for access. Ultrasonography can identify the location of the femoral bifurcation and accessory branches arising above the main common femoral artery bifurcation, and can decrease the chances of an arteriotomy below the bifurcation. Prior analyses of access strategies suggest that an ultrasound-guided technique is associated with fewer overall complications (including hematoma), reduced unintended venipuncture, and improved likelihood of first-attempt success [16, 17]. In our experience, ultrasound visualization can sometimes bias toward a higher or more cranial arteriotomy site with operators less experienced with ultrasound-guided access. However, combining fluoroscopic definition of the anatomic landmarks (the superior and inferior borders of the femoral head) with ultrasound guidance can be assistive in preventing «drift» of the ultrasound probe toward the retroperitoneum. A generous skin nick prior to tract dilation aids in passage of the sheath though the subcutaneous tissue as well as creating a tract for extraluminal blood to allow early detection of postprocedural bleeding.

Inability to pass the sheath over the wire represents a relatively frequent complication of femoral arterial access. This is mainly encountered in patients with morbid obesity and a large amount of subcutaneous tissue to traverse, patients with fibrotic tissue as a result of multiple femoral procedures, or in highly calcified vasculature. When encountering resistance while advancing the arterial sheath over the guidewire, care must be taken not to kink the guidewire by applying excessive force. Proper positioning of the guidewire should be assessed using fluoroscopy to confirm that the guidewire tip is intravascular, and with enough of the wire intravascular to provide «purchase» to introduce the sheath. The sheath should be removed, and while maintaining compressive hemostasis, serial dilation can be performed using progressively larger-bore dilators to create enough of a passage through the subcutaneous tissue or calcified vasculature for the sheath to be advanced. Dilators can also be used to exchange the guidewire for a stiffer wire such as a Supracore to provide the operator with more support in the proximal vasculature to deliver dilators and sheaths. When inserting the sheath or dilator, we recommend not only applying continuous pressure to the dilator or sheath but also applying a twisting motion at the same angle of needle access to optimize the likelihood of passage. Twisting provides a measure of blunt dissection with the sheath tip, while maintaining the same angle of initial needle entry minimizes the misalignment of applied force to the subcutaneous tissue rather than the needle tract itself. Finally, in obese patients with large amounts of subcutaneous tissue, compression of the tissue above the arteriotomy during palpation of the pulse or ultrasonographic identification of the vessel can distort the needle tract, and it may be necessary to re-apply similar compression when passing the sheath. Ultimately, if sheath passage is unsuccessful, vigorous manual or FemoStop mechanical compression can prevent the need for surgical exploration for repair of the arteriotomy.

Intraprocedural strategies to reduce bleeding include weight-based anticoagulation goals and use of the smallest effective sheath size. When anticoagulation is required during PCI, regular monitoring of the activated clotting time (ACT), with a goal of 250–300 s when used alone or 200–250 s when used with a glycoprotein (GP) IIb/IIIa inhibitor, is recommended [13]. While use of bivalirudin has been an effective bleeding reduction strategy, with decreased major bleeding [18, 19, 20], it has also been associated with an increased signal of stent thrombosis. Furthermore, while reduced bleeding was demonstrated in the EUROMAX and HORIZONS-AMI trials, the comparator arm for bivalirudin was unfractionated heparin with GPIIb/IIIa inhibitor use. Contemporary data comparing unfractionated heparin alone with bivalirudin demonstrated similar rates of bleeding with both anticoagulant strategies in one randomized trial [21], while another still found a net decrease in bleeding in patients treated with bivalirudin although the comparison arm had higher weight-based dosing of unfractionated heparin [22]. Our practice has been to transition to unfractionated heparin alone for the majority of procedural anticoagulation, with a weight-based approach of 70 units per kilogram of unfractionated heparin, similar to that used in HEAT-PPCI, and to ensure that the closing ACT (at the conclusion of the procedure) is longer than 250 s in the absence of bailout GPIIb/IIIa use.

Postprocedural bleeding prevention strategies focus on early sheath removal, careful hemostasis technique, and maintaining immobilization following hemostasis. A longer indwelling sheath time is associated with increased bleeding complications, and sheath removal should be performed as soon as is safely possible. Guideline recommendations call for waiting for an ACT less than 150–180 s before sheath removal [13]. If low molecular weight heparin is used, the sheath can be removed 6–8 h after the last dose.

At the time of decannulation, manual pressure is applied with the fingertips proximal to the site of skin entry to account for the subcutaneous course of the needle and to ensure focal occlusive pressure at the arteriotomy site. Once hemostasis is achieved, the patient must remain in the recumbent position with a straightened leg for several hours. One hour per French sheath size is a common general rule of thumb. In patients receiving anticoagulation for other causes, anticoagulation should not be restarted until hemostasis has been demonstrated, weighing the risks of thrombosis against the risk of hemorrhage. The timing and modality of anticoagulation should be considered on a patient-by-patient basis, with indications for anticoagulation (i.e., mechanical mitral valve versus atrial fibrillation with a low CHADS2-VASc score) carefully considered.

Closure devices can be useful for patients with large sheath sizes or anticoagulation used during the procedure, and are associated with decreased time to hemostasis and ambulation [23]. However, it is important to note that closure devices have not been proven to reduce vascular complications overall and are not recommended to be used routinely for diagnostic coronary angiography [13]. If use of a closure device is considered, angiography of the femoral arterial sheath in an ipsilateral oblique view should be performed to confirm that the arteriotomy site is above the arterial bifurcation and not in a diseased segment, so that a closure device can be safely deployed.

In general, risk of bleeding complications can be minimized by optimizing patient selection, utilizing the lowest effective sheath size, careful anticoagulant monitoring with weight-based dosing and predefined ACT goals, early sheath removal, and use of the recumbent position following decannulation.

29.2.2 Arterial Dissection

An arterial dissection is a tear in the intima of an artery and occurs in fewer than 0.2% of cases [2]. This most commonly occurs due to the passage of a guidewire into the subintimal space during arterial puncture with partial cannulation of the arterial lumen with the access needle, wherein only a portion of the needle bore is within the lumen and the other portion is within the vessel wall. Subsequent passage of the guidewire can result in dissection, tearing along tissue planes in the subintimal space. Alternatively, following cannulation the arterial sheath tip can abut the vessel wall such that the force of passing a wire or contrast injection can result in an intimal tear (◘ Fig. 29.5). Immediate recognition of inappropriate resistance to passing the wire can minimize the risk of dissection or limit the size of a dissection plane once present. Additionally, when injecting contrast through the side port of a sheath, it is advisable to have a supportive wire in place to «lift» the sheath tip off a vessel wall in the case of tortuous anatomy.
Fig. 29.5

a Common femoral sheath placed for arterial access. b Contrast injection without a wire in place, showing a patent distal lumen. c Femoral catheter inadvertently retracted (arrow). d Repeat contrast injection demonstrating arterial dissection, stemming from either the initial injection or inadvertent retraction and advancement of the sheath

Management of an arterial dissection depends on the size and direction of dissection. If access is obtained retrograde, the dissection may not obstruct flow. In this case, arterial pressure and antegrade flow can «tack down» the dissection flap. If a dissection is flow limiting, contralateral access is required for balloon angioplasty to seal the flap and may require stent placement, depending on the location of the lesion. In select peripheral procedures with antegrade femoral access, antegrade flow can exacerbate a dissection flap, leading to occlusion, and endovascular intervention is more likely to be needed. Repeated angiography to image the dissection should be carefully considered, as repeated contrast injections can extend the subintimal plane. Finally, it is our practice to avoid repeating access to a dissected vessel for approximately 4–6 weeks to allow for healing of the vessel wall, and to avoid cannulating the subintimal plane. Consideration of duplex ultrasonography prior to repeat cannulation or for surveillance is reasonable as well.

29.2.3 Pseudoaneurysm

A pseudoaneurysm is a persistent communication between a pocket of a hematoma and the artery lumen, which occurs when an arteriotomy site does not properly heal. A pseudoaneurysm has been estimated to form in 0.4% of PCI cases [2]. A pseudoaneurysm most commonly presents as a tender groin mass. On examination, it can be differentiated from a hematoma by the presence of pulsation and a femoral bruit, though these are not always present. Duplex ultrasonography has excellent diagnostic sensitivity (94%) and specificity (97%) [24] (◘ Fig. 29.6).
Fig. 29.6

Arterial duplex ultrasound of the right common femoral artery with Doppler flow (left) indicating a pseudoaneurysm neck connecting the arterial lumen to a larger pocket (right) within the hematoma

Risk factors for pseudoaneurysm formation include low or high arterial puncture sites, poor arterial compression, female gender, obesity, older age, sheath size greater than 8F, peripheral arterial disease, hemodialysis, anticoagulation and antiplatelet use, simultaneous arterial and venous cannulation, and more complex interventions such as coronary stenting, atherectomy, repeat angioplasty, and intraprocedural thrombolytic therapy [24].

A large pseudoaneurysm can cause nerve and vessel compression, leading to neuropathy, claudication, venous thrombosis and, rarely, limb ischemia. The main risk of pseudoaneurysm formation is rupture and subsequent hemorrhage. The management strategy depends on size as the risk of rupture increases with the diameter. If the pseudoaneurysm is less than 2 cm and the patient has no significant discomfort, it can be managed expectantly or with firm compression, as approximately one half of pseudoaneurysms are expected to spontaneously close within a month [24, 25]. The effect of dual antiplatelet therapy on spontaneous closure is not completely known; however, anticoagulation has been associated with a decreased rate of closure and greater likelihood of needing surgical repair [25]. If the pseudoaneurysm is larger than 2 cm, or is causing significant pain, ultrasound-guided thrombin injection is the treatment of choice, with a high rate of success and a low rate of complication (1.3%) in experienced hands [24]. This can be performed by an interventional radiologist or by an operator familiar with the procedure under ultrasonographic guidance. Importantly, the exact location and extension of the pseudoaneurysm, as well as the diameter of the aneurysm neck, must be clearly identified on ultrasound images before injecting the coagulant. After identification of both the pseudoaneurysm sac and neck by ultrasonography, the coagulant is injected into the sac, with care taken to avoid the neck and artery. If these are not visualized and readily identifiable, coagulant should not be injected. Inadvertent intra-arterial injection or intra-arterial propagation of thrombus from injection of the pseudoaneurysm neck represent an extremely rare but serious complication requiring immediate surgical and frequently hybrid revascularization. Ultrasound-guided compression is an alternative strategy though it is associated with significant discomfort. If conservative measures fail and the pseudoaneurysm is persistent, rapidly expanding, infected, or causing compression syndrome, surgical management is indicated [24].

29.2.4 Arteriovenous Fistula

An arteriovenous (AV) fistula is a vascular communication that develops between an artery and an adjacent vein. Risk factors include low arterial puncture or puncture of both the artery and vein, multiple punctures, left-sided puncture, female gender, hypertension, and removal of the arterial and venous sheath at the same time. AV fistula formation has been estimated to occur in 0.86% of cases [26, 27]. The majority of AV fistulas are small, asymptomatic, and hemodynamically insignificant. Rarely, if an AV fistula is high flow, an arterial steal syndrome or high-output heart failure can develop. In retrospective studies, 38% of AV fistulas closed spontaneously within 1 year, most within 4 months [27]. Thus conservative management with duplex is a reasonable approach. If an AV fistula does not close spontaneously, the first-line therapy is ultrasound-guided compression at the site. If a hemodynamically significant AV fistula is persistent despite conservative measures, options include covered stent placement, coil embolization, or surgical intervention.

29.2.5 Femoral Arterial Thrombosis and Embolization

Arterial embolization can occur from thrombus formation on guidewires, within catheters, or at an arterial sheath that embolizes. Vascular closure devices may be also associated with thrombus formation. Arterial thrombosis can lead to acute limb ischemia, though this is fortunately rare, with a reported incidence of <1% [28]. Arterial embolization presents with classic signs of acute limb ischemia: pain, pallor, paresthesia, pulselessness, paralysis, and poikilothermia. The diagnosis is confirmed by arterial duplex. Risk factors for arterial embolization and peripheral occlusion include a small arterial lumen, large sheath size, long sheath indwelling time, prolonged manual compression, cardiomyopathy, older age, hypercoagulable state, arterial dissection, and use of closure devices. Acute limb ischemia is a vascular emergency, and alternative access with angiography of the affected limb should be obtained as soon as possible. Occlusion can be treated using endovascular approaches, with combinations of thrombectomy, catheter-directed thrombolysis, balloon angioplasty, and stenting. If percutaneous methods fail, surgical thrombectomy and bypass should be pursued.

29.2.6 Infection

Infection following percutaneous intervention is rare, with a reported incidence of postprocedural bloodstream infection of 0.1–0.6% [29, 30]. The most common organisms are Staphylococcus aureus and coagulase-negative staphylococci [29]. Infection can present with classic signs and symptoms, including fever, swelling, erythema, pain, and purulence at the access site. Severe infection of the arteriotomy site can cause significant morbidity and mortality with progression to systemic infection or loss of the limb. If infection is suspected, blood cultures, ultrasound imaging, and an infectious disease consultation should be obtained. If no abscess is present, infection can be frequently managed medically with antibiotics. However, in the presence of abscesses, pseudoaneurysm, or persistent bacteremia, surgical wound revision is required. The risk of infection is believed to increase with early reuse of an initial puncture site [30], prolonged retention of a femoral sheath, use of a closure device, presence of hematoma or pseudoaneurysm, an immunocompromised patient, or poor local skin care.

29.2.7 Femoral Closure Device Complications

Closure devices can decrease the time to hemostasis though they have not been shown to decrease vascular complications, and their use can predispose the patient to unique complications. The most common types of closure devices are suture based, collagen plug based, or nitinol clip based. Unsuccessful deployment or failure to achieve immediate access site hemostasis varies between devices and has been reported to occur in 2.1–9% of procedures. Device failure is associated with significantly higher rates of major and minor vascular complications as compared with successful deployment [31].

Closure device complications include femoral arterial stenosis or occlusion, pseudoaneurysm, failure to deploy, late failure with subsequent hemorrhage, and infection. Risk factors for closure device complications include high or low punctures, moderate to severe peripheral arterial disease at the sheath site, small femoral artery diameter (<4–5 mm), and a history of immunodeficiency. For collagen devices, a history of allergy to collagen, beef products, polyglycolic, or polylactic acid polymers are additional risk factors for complications.

A closure device should not be deployed if the arteriotomy site is below the femoral bifurcation or in a diseased segment of vessel. In vessels with significant vascular disease, closure devices can encroach on an already reduced luminal size and result in significant stenosis; the most severe cases can result in thrombosis and acute limb ischemia (◘ Fig. 29.7). Additionally, calcified lesions at the arteriotomy site may limit the effectiveness of closure devices, resulting in early or late device failure.
Fig. 29.7

Subtraction femoral angiogram prior to closure device deployment (left). After the patient develops acute pain in the lower extremity following closure device deployment, repeat angiography (right) demonstrates acute closure of the common femoral artery, secondary to the device deployment

Closure device infection has been reported in 0.3% of cases. Infection can be limb and life threatening with reported mortality as high as 6% [32]. Mycotic pseudoaneurysm was the most common infectious complication and presented a median of 8 days after device insertion, with classic systemic and local signs of infection. Staphylococcus aureus was the most common isolate responsible for 75% of infections, with diabetes being the most common associated comorbidity [32].

The majority of bleeding and ischemic complications from closure devices can be managed by percutaneous approaches. However more severe intravascular complications such as lifted dissection planes, a completely thrombosed or occluded artery from suture-mediated closure, and intravascular device material are more difficult to manage by an endovascular approach and may require surgical intervention.

29.3 Radial Access Complications

Transradial catheterization has been increasingly used for diagnostic and interventional cardiac procedures [33]. Transradial access has been associated with a lower incidence of major access site complications compared with the transfemoral approach [34], and its use to reduce access site complications has been supported by consensus guidelines [13].

29.3.1 Bleeding and Hematoma

Radial arterial access is associated with an overall low risk of major bleeding complications, occurring in fewer than 1% of cases [34]. However, in the limited anatomic space of the forearm, any bleeding is potentially significant as it can progress to compartment syndrome. Fortunately compartment syndrome is a rare complication, reported to occur in 0.004% of cases [35]. Bleeding can occur at the arteriotomy site or at a more proximal vessel from perforation by a guidewire or catheter. Tactile attention to resistance when passing a guidewire can identify passage into a branch vessel and minimize bleeding that may result from advancing further.

Treatment of significant forearm bleeding begins with immediate reversal of anticoagulation and local compression. If a hematoma near the wrist cannot be controlled with a transradial (TR) band, a second TR band can be placed proximally. If this is unsuccessful, or there is concern about active bleeding or compartment syndrome, a blood pressure cuff can be inflated to tourniquet the arm proximally as a temporizing measure while making arrangements to return to the catheterization laboratory to access the limb and perform internal balloon tamponade. If endovascular attempts fail, vascular surgery may be required.

Compartment syndrome is the most serious concern associated with a radial artery hematoma or hemorrhage. Forearm bleeding and pressure buildup into a non-expandable space can progress to occlusion of the radial and ulnar arteries, with resultant ischemia of the hand. Compartment syndrome is diagnosed clinically. Pain, pallor, poikilothermia, paresthesia, pulselessness, and paralysis are symptoms of compartment syndrome; however, the diagnosis should be made prior to all signs being present. When it is diagnosed, a fasciotomy must be performed emergently to prevent long-term ischemic injury (◘ Fig. 29.8).
Fig. 29.8

Upper extremity after emergent fasciotomy and subsequent skin grafting for compartment syndrome secondary to radial access bleeding

29.3.2 Radial Artery Occlusion

Radial artery occlusion (RAO) is the most common complication of radial access and is estimated to occur in 1–10% of cases [36]. RAO is believed to be caused by intimal abrasion and vessel injury in the setting of flow cessation during hemostasis. The risk of RAO increases with small radial artery size and prolonged complete compression during hemostasis [36]. The majority of these cases are asymptomatic, given the collateral circulation of the hand, with only 0.2% of cases becoming symptomatic [36]. When symptomatic, RAO can present with forearm pain, loss of hand grip strength, and paresthesia. RAO precludes repeat use of that site for future catheterizations, as well as preventing future use of the artery as a bypass conduit. RAO is usually managed with observation alone, as the majority of cases will recanalize within 30 days and are asymptomatic. In cases of significant symptoms, recanalization of an occluded segment via an approach from the distal radial artery or from the brachial artery has been described [37, 38], although this should be reserved for extreme cases where conservative management has failed. The use of intraprocedural unfractionated heparin (generally 2000–5000 units), a low sheath-to-artery size ratio, and patent hemostasis have been shown to lower the risk of RAO.

29.3.3 Radial Artery Spasm

Radial artery spasm has been estimated to occur in up to 15% of radial cases [39] and presents as tactile resistance to passing catheters and patient arm discomfort during angiography or sheath removal. The strongest risk factors for spasm are small-diameter radial arteries, radial artery anomalies, multiple catheter exchanges, female gender, and diabetes [39]. Spasm rarely leads to serious complications, though it can result in procedural failure. Prevention of radial artery spasm includes adequate local anesthesia, sedation, intra-arterial vasodilators, and use of a hydrophilic sheath. When access is obtained, a vasodilator cocktail should be administered though the sheath; 2.5 mg of verapamil with 200 mcg of nitroglycerin is commonly used in our laboratory for patients with adequate blood pressure who are without contraindications such as significant bradycardia or severe valvular disease [40]. If severe radial artery spasm and catheter entrapment occur, one can use systemic vasodilators, arm heating, and increased sedation to relieve the entrapment. In rare, severe cases where vasodilators fail and the catheter is unable to be removed, general anesthesia may be required to vasodilate the vessels adequately for safe decannulation.

29.3.4 Radial Artery Pseudoaneurysm

Radial pseudoaneurysm is a rare complication, which generally presents as a pulsatile mass several days to weeks following the procedure and is believed to be caused by incomplete arteriotomy compression. The diagnosis is confirmed by Doppler ultrasound. Multiple puncture attempts, infection, aggressive anticoagulation, and use of larger sheath sizes are believed to increase the risk of developing a radial artery pseudoaneurysm. As with femoral arterial pseudoaneurysm formation, treatment options include ultrasound-guided or radial band compression, percutaneous thrombin injection or, if these fail, surgical excision [41].

29.3.5 Sterile Granuloma

A sterile granuloma is a chronic inflammatory fibrosis with a giant cell reaction around retained foreign body material following the use of a hydrophilic radial sheath. The mechanism by which this occurs is believed to be due to stripping of the hydrophilic coating and its retention under the skin, where it triggers an inflammatory response. A sterile granuloma will present as localized erythema, swelling, and sterile discharge 2–3 weeks following radial access. The true incidence is not known, as it is frequently mistaken for other conditions such as an infected pseudoaneurysm or abscess. If suspected, an ultrasound examination should be performed to exclude true pseudoaneurysm. There is no accepted standard for treatment, though if no fever or leukocytosis is present, these can likely be managed expectantly [42].

29.3.6 Other Rare Complications

AV fistula formation at the radial site is extremely uncommon. A radial AV fistula presents as pain and swelling at the puncture site with visibly dilated veins and a palpable thrill. Surgical repair may be required for symptomatic patients. Neuropathy is also a very rare complication of radial artery access and can manifest as digital paresthesia [43].

29.4 Brachial Access Complications

The rates of brachial artery access bleeding complications and procedural success are comparable to those observed with the femoral approach in experienced users [44]. However, low-volume operators have higher rates of complications than experienced operators [45]. Given that the brachial approach is less frequently used, interoperator variability of complication rates can be expected. Major complications include pseudoaneurysm, hematoma, median nerve dysfunction, and brachial artery thrombosis. Brachial artery thrombosis can be managed by either endovascular or open surgical revascularization strategies.

29.4.1 Brachial Artery Thrombosis

Brachial artery thrombosis has been reported to occur in fewer than 2% of cases [46]. The brachial artery is a terminal artery without collateral circulation, thus thrombosis can potentially lead to limb-threatening occlusion. The risk of thrombosis increases with female gender and larger sheath size [46, 47]. If brachial artery thrombosis occurs, immediate endovascular or surgical intervention is required to restore flow and avoid permanent nerve injury or limb loss.

29.4.2 Brachial Hematoma and Bleeding

Brachial artery access was associated with entry-related bleeding complications in 2.3% of cases in the ACCESS trial [44]. As with radial artery access, any bleeding into the upper arm is potentially significant and can progress to compartment syndrome or irreversible median nerve injury. If present, immediate intervention with anticoagulation reversal and compression of the arteriotomy site is required. Large hematomas may require surgical excision.

29.5 Summary

Access site complications will offset procedural success and lead to poor patient outcomes. It is essential for the interventional cardiologist to employ meticulous access technique and bleeding reduction strategies to optimize access safety. Routine individualized risk factor assessment prior to the procedure should guide appropriate patient selection, optimization of modifiable factors, and choice of access site approach. The transradial technique is preferred when possible, and when not, a methodical and standardized approach to transfemoral access should be taken. Meticulous technique to ensure femoral artery cannulation at the level of the mid–femoral head, minimizing the arteriotomy size using the smallest needed equipment, and maintaining a stable intraluminal position, as well as employing a goal-directed anticoagulation strategy with careful monitoring of ACT, can reduce intraprocedural complications. Finally, careful attention to hemostatic techniques and prompt recognition and management of complications are key aspects of postprocedural care. Adopting and integrating bleeding reduction strategies into all phases of procedural planning can decrease the most common types of access site complications. Dedication to the technical training of operators, wider education in and adoption of bleeding reduction strategies, participation in multicenter registry data collection to track outcomes and establish best practices, and improving ward staff awareness of the presenting signs of access complications can further minimize the incidence and impact of these complications going forward.


  1. 1.

    In most cases a 5–10 mg test dose is initially administered to assess for an anaphylactic reaction prior to the full dose. Allergic reactions have been associated with prior use of neutral protamine Hagedorn (NPH) insulin, past vasectomy, and fish hypersensitivity.



We would like to thank and acknowledge Stephen W. Waldo, MD, Ehrin J. Armstrong, MD and John C. Messenger, MD for their support, guidance and mentorship.


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Copyright information

© Springer International Publishing AG, part of Springer Nature 2018

Authors and Affiliations

  1. 1.Department of Cardiology, University of Colorado School of MedicineAuroraUSA
  2. 2.Veterans Affairs Eastern Colorado Health Care SystemDenverUSA

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