complications at femoral vascular access sites in...

contribute to the occurrence offemoral vascular access site compli-cations (VASCs), including hematoma,retroperitoneal hemorrhage, pseudo -aneurysm, arteriovenous fistula, arte-rial occlusion, femoral neuropathy,and infection. This article specificallyaddresses patients undergoing PCIfor acute coronary syndrome or non–ST-segment-elevation myocardialinfarction (NSTEMI) and discusseshow nurses can be instrumental inoptimizing patients’ outcomes.

The reported incidence of VASCsduring PCI is from 5.4% to 20%,2-6

depending on the definition andcriteria used. VASCs remain animportant source of increased mor-bidity,7-9 mortality,2,6,9-11 length ofstay,4,6 and cost.2,4 The economic ram-ifications of VASCs are significant.Jacobson et al4 reported that the costof PCI when bleeding complicationsarose was more than double the

Managing Risk ofComplications atFemoral VascularAccess Sites in Percutaneous Coronary Intervention

Cover Article

Nakia Merriweather, RN, MSNLinda M. Sulzbach-Hoke, RN, PhD, CCNS, ACNS-BC, CCRN

Percutaneous coronaryintervention (PCI) hasreduced morbidity andmortality from cardio-vascular disease. In 2009,

an estimated 596000 PCI procedureswere performed.1 Major advances inPCI have included increasingly com-plex antiplatelet and antithromboticregimens used in conjunction withPCI. Unfortunately, although theseadvances yield benefits, they also

Percutaneous coronary intervention for acute coronary syndrome or non–ST-elevation myocardial infarction requires the use of potent oral and intravenous anti -platelet and antithrombin medications. Although these potent antithrombotic agentsand regimens may increase the effectiveness of percutaneous coronary intervention,they are also generally associated with an increased risk of vascular access complicationssuch as hematoma, retroperitoneal hematoma, pseudoaneurysm, arterial occlusion,and arteriovenous fistula, which in turn are associated with increased morbidity, mor-tality, and costs. Risk factors predisposing patients to these complications are bothmodifiable (procedure technique, medications, hemostasis method) and nonmodifiable(sex, age, body mass index, blood pressure, renal function). Patients’ risks can bereduced by nurses who are knowledgeable about these risk factors and identify com-plications before they become problematic. (Critical Care Nurse. 2012;32[5]:16-30)

This article has been designated for CNE credit.A closed-book, multiple-choice examinationfollows this article, which tests your knowledgeof the following objectives:

1. Identify factors contributing to complications related to vascular access sites2. Describe the different types of anticoagulation used before, during, and after percutaneous coronary intervention 3. Define the methods of attaining hemostasis in patients undergoing percutaneous coronary intervention

CNEContinuing Nursing Education

©2012 American Association of Critical-Care Nursesdoi: http://dx.doi.org/10.4037/ccn2012123

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by AACN on June 13, 2018http://ccn.aacnjournals.org/Downloaded from

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costs of uncomplicated PCI ($25 371vs $12279).4 Interventions aimed atreducing the risk of adverse eventsare likely to improve both financialand clinical outcomes.

Removing femoral sheaths andmanaging related complications afterPCI are predominantly the responsi-bilities of nurses in many acute andcritical care settings.3,5,12,13 Therefore,it is essential for nurses to understandthe causes of and predisposing riskfactors for VASCs. These risk factorscan be categorized as modifiableand nonmodifiable.

Modifiable Risk FactorsThe primary modifiable risk

factors for VASCs are femoral access;medications administered before,during, and after the procedure; andhemostasis method. Although theinterventional cardiologist controlsthe femoral access and medicationsordered, the hemostasis method iscontrolled by the nurse unless avascular closure device is deployed.

Femoral AccessPercutaneous entry through

the femoral artery and veinapproach for PCI is preferredbecause of the large diameter ofthose vessels,14 which improves thespeed and simplicity of the proce-dure.15 VASCs at the femoral site

are often associated with the loca-tion of the femoral puncture,7,15,16

the number of attempts,7,16 and

catheter size17 (Table 1). To facilitatevessel entry and effective compres-sion, the puncture should be abovethe femoral bifurcation but 1 or 2 cmbelow the inguinal ligament,7,8,15,19

which extends from the anteriorsuperior iliac spine to the pubictubercle (Figure 1). Many majorand potentially lethal VASCs arerelated to punctures either too highor too low below the inguinal liga-ment.8 Table 2 describes the clini-cal findings of VASCs and theassociated management.

Nakia Merriweather is a cardiology nurse in the echocardiography laboratory at the Hospitalof the University of Pennsylvania, Philadelphia.

Linda M. Sulzbach-Hoke is a clinical nurse specialist on a 48-bed progressive care unit at theHospital of the University of Pennsylvania, providing nursing care to adult cardiac patients.Her research and several of her publications support evidence-based nursing practice, specifi-cally in patients undergoing percutaneous coronary intervention.

Authors

Corresponding author: Linda Hoke, Cardiac Intermediate Care Unit, Founders 10, Hospital of the University ofPennsylvania, 3400 Spruce Street, Philadelphia PA 19104 (e-mail: [email protected]).

To purchase electronic or print reprints, contact The InnoVision Group, 101 Columbia, Aliso Viejo, CA 92656.Phone, (800) 899-1712 or (949) 362-2050 (ext 532); fax, (949) 362-2049; e-mail, [email protected].

Table 1 Femoral puncture location and associated complicationsa

Femoral puncture location: definition

Low stick: puncture below the femoral bifurcation

High stick: puncturing the inferior epigastric artery

Posterior wall puncture: puncture through the backwall of the artery

Complications

PseudoaneurysmHematomaArteriovenous fistula

Retroperitoneal hemorrhage

Retroperitoneal hemorrhage

a Based on data from Turi,7 Ragosta,8 Baim and Simon,15 Kamineni and Butman,18 and Rashid and Bailey.19

Figure 1 Anatomical landmarks in relation to the femoral vessels.

Inguinalligament

Superficialfemoral artery

Inferiorepigastric

artery

Femoralvein

Profundafemoris

Commonfemoral artery

Exterioriliac artery

www.ccnonline.org CriticalCareNurse Vol 32, No. 5, OCTOBER 2012 17



Table 2 Vascular access site complications and management

Complication

Hematoma

Incidence: 5% to 23%20

Retroperitonealhemorrhage

Incidence: 0.15% to 0.44%20

Pseudoaneurysm

Incidence: 0.5% to 9%20

Arteriovenous fistula

Incidence: 0.2% to 2.1%20

Management

Apply pressure to site21

Mark the area to evaluate for anychange in size21

Provide hydration21

Monitor serial complete blood cellcounts21

Maintain/prolong bed rest21

Interrupt anticoagulant andantiplatelet medications if necessary21

Blood transfusion, if indicated21

If severe, may require surgicalevacuation20

Many hematomas resolve within afew weeks as the blood dissipatesand is absorbed into the tissue21

Provide hydration21

Perform serial blood cell counts21


Interrupt anticoagulant and anti -platelet medications if necessary20

Blood transfusion, if indicated14

If severe, may require surgicalevacuation20


Small femoral pseudoaneurysmsshould be monitored; they com-monly close spontaneously aftercessation of anticoagulant therapy20

Large femoral pseudoaneurysmscan be treated by ultrasound-guided compression, surgicalintervention, or ultrasound-guidedthrombin injection21

Some arteriovenous fistulasresolve spontaneously withoutintervention21

Some arteriovenous fistulasrequire ultrasound-guided compression or surgical repair20

Continued

Clinical findings

Swelling surrounding the puncturesite (visible)21

Area of hardening under the skinsurrounding the puncture site (palpable)21

Varies in size20

Often associated with pain in thegroin area that can occur at rest orwith leg movement22

Can result in decrease in hemoglobinand blood pressure and increase inheart rate, depending on severity22

Moderate to severe back pain22

Ipsilateral flank pain20

Vague abdominal or back pain22

Ecchymosis and decrease in hemoglobin and hematocrit arelate signs21

Abdominal distention21

Often not associated with obviousswelling21

Hypotension and tachycardia20

Diagnosed by computed tomography20

Swelling at insertion site22

Large, painful hematoma21

Ecchymosis22

Pulsatile mass22

Bruit and/or thrill in the groin22

Pseudoaneurysms can rupture, caus-ing abrupt swelling and severe pain21

Suspect nerve compression whenpain is out of proportion to size ofhematoma21

Nerve compression can result inlimb weakness that takes weeksor months to resolve21

Diagnosed by ultrasound20

Can be asymptomatic14

Bruit and/or thrill at access site20

Swollen, tender extremity22

Distal arterial insufficiency and/ordeep venous thrombosis can resultin limb ischemia21

Congestive heart failure20

Confirmed by ultrasound21

Description

The most common vascularaccess site complication

A collection of blood located inthe soft tissue21

Occurs because of blood loss atthe arterial and/or venous accesssite or perforation of an arteryor vein22

May occur if the arterial punctureis below the femoral bifurcationso the femoral head is notavailable to assist with com-pression7,8,15,18

Bleeding that occurs behind theserous membrane lining thewalls of the abdomen/pelvis21

May occur if the arterial wallpuncture is made above theinguinal ligament, resulting inperforation of a suprainguinalartery21 or penetration of theposterior wall7,8,15

Can be fatal if not recognizedearly21

A communicating tract betweenthe tissue and, usually, one ofthe weaker walls of the femoralartery, causing blood to escapefrom the artery into the sur-rounding tissue14

Possible causes include difficultywith arterial cannulation, inade-quate compression after sheathremoval, and impaired hemo-stasis21

May occur if the arterial punctureis below the femoral bifurcationso the femoral head is notavailable to assist with com-pression7,8,15,18

A direct communication betweenan artery and a vein that occurswhen the artery and vein arepunctured14

The communication occurs oncethe sheath is removed20

Risk factors:Multiple access attempts7

Punctures above or below proper site level7

Impaired clotting21




High sticks are significantly linkedwith retroperitoneal hemorrhageresulting from the likelihood ofpuncturing the inferior epigastricartery.7,8,15,18,19 However, puncturesbelow the proper access points donot eliminate the risk of retroperi-toneal hemorrhage; penetration ofthe posterior wall of the artery dur-ing femoral puncture can also causeretroperitoneal bleeding (Table 1).7,8,15

Low sticks can predispose patientsto pseudoaneurysm, hematoma, andarteriovenous fistula.7,8,15,18,19 Whenthe groin is accessed at or below thelevel of the femoral bifurcation, thefemoral sheath is put into vessels thatare smaller than the common femoral

artery. Depending on the size of thesheath used, these vessels may not belarge enough to accommodate thesheath. As a result, access below thefemoral bifurcation is more likely tolead to a VASC.7,8,15,18 When the groinsite is accessed under optimal condi-tions, the femoral head can be usedafter sheath removal to achieve effec-tive compression of the site and pre-vent bleeding complications. Withlow sticks, the femoral head is notavailable to assist with compression.Instead, pressure is placed againstsoft tissue, making effective hemosta-sis less probable. This can predisposepatients to hematoma and pseudo -aneurysm.7,8,15,18 Finally, low sticks are

near the bifurcation vessels to otherblood vessels. Various vein branchesthat run along or anterior to thebifurcation may be accessed duringarterial puncture, resulting in anarteriovenous fistula.7,8,15,18

Repeat or multiple punctures ofthe artery increase the likelihoodthat another artery or vein will bepunctured, causing the developmentof VASCs.7 Increased sheath sizeincreases the risk for vascular traumaand VASCs. Grossman and col-leagues17 found that PCIs performedwith 7F and 8F guides comparedwith 6F guides were associated withmore use of contrast medium, renalcomplications, bleeding, VASCs,

Table 2 Continued

Complication

Arterial occlusion

Incidence: <0.8%20

Femoral neuropathy

Incidence: 0.21%23

Infection

Incidence: <0.1%20

Management

Treatment depends on size/type ofembolus, location, and patient’sability to tolerate ischemia inaffected area20

Small thromboemboli in well-perfused arterial areas mayundergo spontaneous lysis20

Larger thromboemboli may requirethromboembolectomy, surgery,and/or thrombolytic agents20

Distal embolic protection devices (ie,filters) may be placed if necessary21

Identification and treatment of thesource23

Treatment of symptoms23

Physical therapy23

Treatment of symptoms (eg, pain)21

Antibiotics20

Clinical findings

Classic symptoms include the 5 Ps:Pain22

Paralysis20

Parasthesias22

Pulselessness22

Pallor22

Doppler studies help localize the area20

Angiogram is required to identifyexact location of occlusion site20

Pain and/or tingling at femoral accesssite22

Numbness at access site or furtherdown the leg22

Leg weakness22

Difficulty moving affected leg23

Decreased patellar tendon reflex22

Pain, erythema, swelling at accesssite14

Purulent drainage at access site20

Fever14

Increased white blood cell count21

Description

Occlusion of an artery by athromboembolism20

Most common sources: muralthrombus originating in cardiacchambers, vascular aneurysms,or vascular atheroscleroticplaques20

Thromboemboli can develop atsheath site or catheter tip;embolization occurs duringsheath removal20

Prevention or at least reductioncan be obtained by anticoagula-tion, vasodilators, and nursingvigilance20

Nerve damage caused by injuryof the femoral nerve(s) duringaccess and/or compression ofnerves by a hematoma23

Colonization by a pathogen Causes:

Compromised technique14

Poor hygiene14

Prolonged indwelling sheathtime14

Femoral access closure device(closure devices have beenlinked with increased occur-rence of infection)14




transfusions, major adverse cardiacevents, and deaths.

MedicationsAs techniques for performing

PCI have progressed through theyears, so has the approach to anti-coagulation before, during, andafter the procedure. Combinationsof oral and intravenous antiplateletand antithrombin therapy are uni-versally used for patients withacute coronary syndrome, includ-ing unstable angina and NSTEMI,who are undergoing PCI. Theseagents (shown in Table 3) are criti-cal in reducing rates of mortality,adverse ischemic events (such asrecurrent myocardial infarction),short- and long-term complicationsof PCI, and other major adversecardiac events.35-37

Antithrombins inhibit the coag-ulation factors that act in a com-plex cascade to form fibrin strandsas part of the process of hemosta-sis. The antithrombins consist ofunfractionated heparin (UFH), lowmolecular weight heparin (LMWH),and direct thrombin inhibitors(DTIs; eg, bivalirudin, argatroban).Antiplatelet agents can prevent theformation of blood clots by inhibit-ing the activation of platelets. Inso doing, these agents preventblood clotting, usually in high-flowareas of the circulation such as thearterial circulation. They have lit-tle effect in inhibiting thrombosisin the venous circulation. The anti -platelet agents include glycoproteinIIb/IIIa inhibitors, adenosinediphosphate inhibitors (eg, clopi-dogrel and prasugrel), and aspirin.It is the nurse’s responsibility toknow the mechanism of action ofeach medication, verify and double

a modest excess of bleeding, theadvantages of convenience shouldbe balanced.42,43

Direct Thrombin Inhibitors. DTIsmay be used as an alternative toUFH and LMWH. DTIs exert theireffect by interacting directly withthe thrombin molecule without theneed for a cofactor. Unlike heparin,DTIs do not rely on antithrombin toprovide anticoagulation but func-tion by inhibiting thrombin that isbound to fibrin or fibrin degrada-tion products.44 In addition, unlikeheparin, DTIs have an antiplateleteffect.45,46

Their pharmacokinetic profileprecludes the need to measure acti-vated clotting times during the pro-cedure or before sheath removal.Additionally, it has been reportedthat the most commonly used DTI,bivali rudin, is associated with lowerfrequency of bleeding at the accesssite (4%) than are UFH or LMWH(plus glycoprotein IIb/IIIainhibitors; 7%) in patients undergo-ing PCI (P<.001).47 DTIs offer manyadvantages over heparin, includingthe inhibition of both circulatingand clot-bound thrombin; a morepredictable anticoagulant response;inhibiting thrombin-induced plateletaggregation; and absence of induc-tion of immune-mediated thrombo-cytopenia.44,48

Glycoprotein IIb/IIIa Inhibitors.These inhibitors prevent the finalpathway of platelet aggregation byattaching to fibrinogen and otherproteins, blocking platelet aggrega-tion and preventing thrombosis.39

Three parenteral agents—abciximab,eptifibatide, and tirofiban—are cur-rently approved for clinical use bythe Food and Drug Administration.15

They are often used in conjunction

check the type and dosage of med-ication(s) prescribed, and monitorthe patients’ reactions to the med-ication(s) to reduce VASCs.

Unfractionated Heparin. The anti-coagulant effect of UFH is mediateddirectly by inhibiting thrombin-activated conversion of fibrinogento fibrin. UFH is used to preventthrombosis before and during PCI.Heparin binds to thrombin, pre-venting the conversion of fibrinogento fibrin.38,39 During the PCI, heparinactivity is monitored by measuringactivated clotting time, with a goalof maintaining times greater than200 s.24 Activated clotting time indi-cates the effectiveness of high-doseheparin therapy by measuring theintrinsic clotting activity of the wholeblood. Activated clotting time lackscorrelation with results of othercoagulation tests and is used todemonstrate the inability to coagu-late rather than to quantify theability to clot.

Low Molecular Weight Heparin.LMWH, like UFH, exerts its antico-agulant activity by activating anti -thrombin, which plays a role inrestricting thrombus formation.Although it consists only of frag-ments of UFH, it is just as effectiveand has a half-life 2 to 4 times longerthan that of standard heparin.39

Because LMWH has little effect onmeasurements of activated clottingtime, it should not be used as a guideto anticoagulation therapy.27 Sheathremoval when followed by manualor mechanical compression may beperformed 4 hours after the last intra-venous dose or 6 to 8 hours after thelast subcutaneous dose.28 LMWH isa safe and effective alternative tounfractionated heparin.27,28,40,41

Although some studies have shown




Table 3 Dosing of anticoagulant and antiplatelet agents used in percutaneous coronary intervention (PCI)Drug

Bivalirudin (Angiomax)

Enoxaparin

Unfractionated heparin

Abciximab (ReoPro)

Eptifibatide (Integrilin)

Tirofiban (Aggrastat)

Aspirin

Clopidogrel (Plavix)

Prasugrel

Comments

With addition of 600 mg clopidogrel, can beadministered with or without unfractionatedheparin for antithrombotic treatment in PCIand acute coronary syndrome24

No anticoagulation monitoring available27

Risk for heparin-induced thrombocytopenia26

Only partial reversal with administration of protamine sulfate26

Monitor by using activated partial thromboplas-tin time or activated clotting time at bedside26,29

Reverse with protamine sulfate26

Risk for heparin-induced thrombocytopenia29

Administer with aspirin and heparin30

Platelet aggregation returns to normal 24-48hours after discontinuation26

Monitor activated clotting time, activated partialthromboplastin time, hemoglobin, plateletcount when given with heparin30







Administer as soon as possible after hospitaladmission (if patient has not already takenaspirin)26

Administer to patients not able to take aspirinbecause of hypersensitivity or significant gastrointestinal intolerance26

Use in conjunction with aspirin33

Antiplatelet effects are irreversible34

Takes several days to achieve maximum effective-ness without a loading dose34

Variability in patients’ responsiveness to the drug33

Antiplatelet effects are irreversible26

Little variation noted in patients’ response34

Dosing

Anticoagulant agents

Loading dose: 0.75 mg/kg intravenous bolus (wait 30minutes if patient received unfractionated heparin)

Maintenance dose: 1.75 mg/kg per hour infusion duringPCI24

Loading dose: 30 mg intravenous bolusMaintenance dose: 1 mg/kg subcutaneous every 12 hours If patient received initial anticoagulant therapy <8 hours

before PCI: no additional therapy If last subcutaneous dose >8 hours ago: 0.3 mg/kg intra-

venous bolus25,26

Creatinine clearance <30 mL/min: 1 mg/kg every 24 hours26

Loading dose: 70-100 IU/kg intravenous bolus; if targetvalues for activated clotting time are not achieved,administer additional heparin boluses 2000 to 5000 IU28

Loading dose on glycoprotein IIb/IIIa inhibitor: 60 U/kgintravenous bolus28

Administer for target activated clotting time of 200-250seconds (target activated clotting time may vary bymethod of measurement)24

Dosing must take into account whether patient receivedinitial medical therapy

Intravenous antiplatelet agents

Loading dose: 0.25 mg/kg intravenous bolus Maintenance dose: 0.125 µg/kg per minute (maximum,

10 µg/min) infusion during percutaneous coronary inter-vention and for 12 hours after PCI 30

Loading dose: 180 µg/kg intravenous bolusMaintenance dose: 2 µg/kg per minute during PCI; continue

18-24 hours after PCI Creatinine clearance <50 mL/min: Reduce both loading

and maintenance dose infusion rate by 50%24

Loading dose: 0.4 µg/kg per minute intravenous for 30minutes

Maintenance dose: 0.1 µg/kg per minute infusion duringpercutaneous coronary intervention and continued for18-24 hours after PCI

Creatinine clearance <30 mL/min: Reduce both loadingand maintenance dose infusion rate by 50%24

Oral antiplatelet agents

Daily dose: 162-325 mg daily orally (patients at high riskof bleeding may receive 75-162 mg/d)25,26

Loading dose: 300-600 mg orallyMaintenance dose: 75 mg/d, ideally up to 1 year24

Loading dose: 60 mg orallyMaintenance dose: 10 mg daily for ≥12 months after

stenting24




with UFH or a DTI. The adjunct useof a glycoprotein IIb/IIIa inhibitorduring PCI is effective and associ-ated with improved in-hospital sur-vival rates.49-52 However, the optimaltiming of initiation of glycoproteinIIb/IIIa inhibitor therapy in patientswith unstable angina or NSTEMI(ie, whether to administer therapybefore or after PCI) and the optimalapplication of this therapy have notbeen determined.24,53 The 2011guidelines on PCI from the Ameri-can College of Cardiology Founda-tion/American Heart Association(ACC/AHA) support early adminis-tration of glycoprotein IIb/IIIabefore catheterization for patientswith unstable angina or NSTEMIundergoing PCI who are judgedclinically to be at high risk of thrombotic events relative to bleed-ing risk.24 The guidelines furthernote that much of the research evaluating use of these agents forpatients with STEMI was performedin the era before routine dual oralantiplatelet therapy and was evalu-ated largely by placebo-controlledcomparisons.24

More recently, 3 trials were doneto evaluate glycoprotein IIb/IIIaantagonists as adjuncts to oral anti -platelet therapy in patients withprimary PCI.54-56 The results bringinto question whether glycoproteinIIb/IIIa antagonists provide addi-tional benefit to STEMI patientswho received dual antiplatelet ther-apy before catheterization. TheACC/AHA guidelines judge thatroutine use of glycoprotein IIb/IIIaantagonists for such patients cannotbe recommended, although somepatients (eg, those with a large throm-bus burden or who received inade-quate thienopyridine loading) may

as 30 minutes after administration.64

Prasugrel is superior to clopidogrelin preventing ischemic events inpatients with acute coronary syn-drome undergoing PCI, eventhough there is an associatedgreater risk of bleeding.24,35,57,65 Pra-sugrel therapy should be individual-ized and targeted toward thosepatients with stents or patientswith decreased platelet inhibitionby clopidogrel.57 Patients with a his-tory of cerebrovascular events haveexperienced significant harm fromadministration of prasugrel.35 Pra-sugrel has a black box warning, notto be used in patients with previousstroke or transient ischemic attackbecause of its greater tendency tocause intensive inhibition of plateletaggregation in general and the find-ings of increased levels of bleedingcompared with clopidogrel.66

Aspirin. Aspirin inhibits thecyclo-oxygenase enzyme, whichstops prostaglandin synthesis andrelease, and inhibits prostaglandinsynthetase action, which preventsformation of thromboxane A2, thusinhibiting platelet aggregation.39

Long-term aspirin therapy is recom-mended for patients who undergoany revascularization procedure,including PCI.

Hemostasis MethodsCurrently, 3 main techniques are

used to achieve hemostasis at thefemoral access site after PCI: manualcompression, mechanical compres-sion, and vascular closure devices.

Manual Compression. Manualcompression has been the “goldstandard” for obtaining hemostasisat the vascular access site for years,but this standard has changed as newdevices have come on the market.

benefit. Clinical practices with theseand other antithrombotic agentscontinue to evolve.

Clopidogrel. This oral antiplateletagent specifically inhibits the P2Y12adenosine diphosphate receptor onthe platelet surface, preventing acti-vation of the glycoprotein IIb/IIIareceptor complex, thereby reducingplatelet aggregation.39,57 Plateletsblocked by clopidogrel are affectedfor the remainder of their lifespan(~7-10 days).39 Clopidogrel reducesthe frequency of ischemic complica-tions after PCI and improves postin-tervention outcomes.24,58

Clopidogrel resistance (ie,decreased inhibition of platelet func-tion after administration of clopido-grel) may occur in 30% of patientsand may relate to factors such asbioavailability, noncompliance,underdosing, lower absorption,drug interference, or single nucleotidepolymorphisms.24,57,59 Poor responseto oral antiplatelet agents increasesthe risk of thrombotic events, includ-ing myocardial infarction,60 particu-larly after coronary angioplasty.61

The authors of a recent meta-analysissuspect that the cause of clopidogrelresistance is an interaction with gly-coprotein IIb/IIIa inhibitors and theuse of different cutoffs to identifynonresponders.62

Prasugrel. This novel third-generation rapid-acting thienopyri-dine is a more potent blocker of theplatelet P2Y12 receptor than is clopi-dogrel,57,63 and no resistance has beenreported.57 The 60-mg loading doseachieves faster, more consistent, andgreater inhibition of adenosinediphosphate–induced platelet aggre-gation than does 600 mg clopidogrel.Prasugrel produces a significantlygreater effect than clopidogrel as early




The artery punctured is superior andmedial to the skin puncture site, sopressure is applied as the sheath isremoved by placing the index andmiddle fingers 1 to 2 cm above thesite where the sheath enters the skinand applying pressure as the sheath isremoved (Figure 2).67 Hemostasis isachieved by compressing the femoralartery against the femoral head.

Manual compression for somepractitioners is not an optionbecause it requires strength and theability to hold a good compressionfor 15 to 20 minutes.6,21 If hand andarm fatigue develops during theprocedure, the amount of pressureapplied to the femoral artery mayvary, causing VASCs.3

Mechanical Compression.Mechanical compression involves theapplication of constant pressure onthe artery to obtain hemostasis andallows hands-free catheter removal sothat nurses can monitor the patient.3

There are 2 main types of compres-sion: The C-clamp (CompressAR,Advanced Vascular Dynamics) andpneumatic (FemoStop, Radi MedicalSystems AB, St Jude Medical, Inc).The C-clamp consists of a flat metalplate, placed under the mattress atthe patient’s hip to stabilize thedevice, and a C-clamp arm. A dis-posable translucent pad is attachedto the tip of the C-clamp arm (Fig-ure 3). The FemoStop device uses asmall pneumatic clear pressure dome,a belt placed around the patient’ships, and a pump with a manometermaking it possible to adjust pressureto an optimal level (Figure 4). Aswith manual compression, thetranslucent pad or clear dome isplaced 1 to 2 cm above the site wherethe sheath enters the skin and pres-sure is applied by pressing down on

the C-clamp arm or adjusting thepressure with the pump. Mechanicalcompression does not cause handand/or arm fatigue and is just aseffective as manual compression inobtaining hemostasis.3,5,68 The translu-cent pad or clear dome provides easyvisualization of the puncture sitewhile the pressure is slowly released.It is important to remember thatboth manual and mechanical com-pression can be ineffective in obtain-ing hemostasis in patients whoreceived low sticks.7

Vascular Closure Devices. Thesedevices first appeared in the 1990sas means of reducing time on bedrest and improving both hemostasisand patients’ comfort. A variety ofdevices seek to mechanically closethe arterial puncture site duringsheath removal in the catheterizationlaboratory in fully anticoagulatedpatients and shorten the time tohemostasis and ambulation.15 Threemain types of vascular closure devicescan be categorized by the mecha-nism of hemostasis, including

Figure 2 (A) Once the sheath is removed, external compression is applied 1 to 2 cm above the puncture site. (B) Effective compression was not maintained,causing a hematoma to develop.

— Pulsatile flow

Sheath removalExternal pressure

on arterial puncture(proximal to skin incision)

External compression

A

— Constriction around wound

Skin incision

Puncture tract

Artery

Arterial puncture

Hematoma

Sheath removed

B




sutures, collagenlike plugs, and sta-ples/clips (Figures 5-7).14,19,69 Suture-mediated closure devices tie off thefemoral artery with sutures. Colla-gen plugs seal the puncture site bystimulating platelet aggregation andthe release of coagulation factors,which results in the formation of aclot. Extravascular clips or staples

C-clamp and manual compression,all provide low and comparablecomplication risks following sheathremoval in the era of antiplatelet

are used to seal off the puncture sitein the artery. Hemostasis is usuallyobtained shortly after deployment,allowing the patient to get out ofbed and ambulate faster.14,15,69-72

Vascular closure devices, whencompared with the mechanical

Figure 3 CompressAR C-Clamp.

Courtesy of Advanced Vascular Dynamics, Portland, Oregon.

Figure 4 FemoStop. Pneumaticcompression.

Courtesy of Radi Medical Systems AB, St JudeMedical, Inc, St Paul, Minnesota. Permissionto reproduce these images granted by St JudeMedical, Inc.

Figure 5 Perclose Proglide 6FSuture-Mediated Closure System.

Courtesy of Abbott Vascular, Redwood City,California. ©2010 Abbott Laboratories. Allrights reserved.

Figure 6 AngioSeal, BioabsorbableActive Closure System With anIntra-Arterial Anchor.

Courtesy of Radi Medical Systems AB, St JudeMedical, Inc., St Paul, Minnesota. Permissionto reproduce these images granted by St JudeMedical, Inc.

Figure 7 StarClose Vascular ClosureSystem, Extraluminal Nitinol Clip.

Courtesy of Abbott Vascular, Redwood City, California. ©2010 Abbott Laboratories. All rightsreserved.




and antithrombotic therapies.3,72

Appropriate selection of patients bythe physician is important, and thedevice should be placed only afterconfirmation of the vascular anatomyand the absence of significant localperipheral arterial disease. In cases inwhich vascular closure devices are noteffective, manual compression mustbe applied to accomplish hemostasis.

Nonmodifiable Risk FactorsNonmodifiable risk factors for

VASC are characteristics of patientsthat cannot be changed in the PCIsetting. These include sex, advancedage, body mass index (BMI), hyper-tension, and renal dysfunction. Eachof these factors alone, and especiallyin combination, can affect the likeli-hood that a patient will experience aVASC after a procedure.

SexAn estimated 34% of the almost

600000 PCIs in the United Statesannually are performed in women,and being female has been clearlyidentified as a risk factor forVASCs.7,11,28,73-76 Compared with men,women undergoing PCI are olderand have a higher incidence ofhypertension, diabetes mellitus,hypercholesterolemia, and comorbiddisease.28 A nationwide study of199690 patients showed that womenpresented for PCI with unstableangina and/or NSTEMI more oftenthan men did and had a significantlyhigher frequency of VASCs.77 Thesewomen were older than their malecounterparts, although they hadfewer high-risk angiographic featuresand higher ejection fractions. How-ever, women have been observed tohave atypical and sometimes ambigu-ous symptoms, which may have

reached higher acuity by the timethey arrive at the cardiac catheteri-zation laboratory, thereby contribut-ing to their level of complications.28,78

Advanced AgeAdvanced age, generally more

than 70 years of age, is directlylinked to increased incidence ofVASCs.3,7,11,28,37,73-76,79 Results of a retro-spective study of the incidence, pre-dictors, and prognostic impact ofperiprocedural bleeding and trans-fusion in 10974 patients undergo-ing PCI indicated that age was amongthe strongest predictors of majorbleeding.80 It is generally agreedthat with increasing age, patientsare at increased risk of bleeding com-plications, possibly related to localvascular changes or more advancedvascular disease.81

Body Mass Index Researchers have identified a

lower BMI (calculated as weight inkilograms divided by height inmeters squared) as a risk factor forvascular complications in severalstudies.7,74,76,82 Mehta et al83 studied2325 patients with acute myocardialinfarction who received primaryPCI and reported that althoughobese patients (those with BMI ≥30)had more cardiovascular risk factorsat baseline, they had fewer VASCs,shorter hospital stays, and fewerdeaths in the hospital and at 12months than did patients with anormal BMI. This difference mayhave been because the obese patientswere a mean of 6 years younger thanthe patients with normal BMI orbecause obesity is related to impairedfibrinolysis and increased plateletaggregation.83 Delhaye et al84 furtherexamined the role of BMI in records

of 16783 patients who underwentPCI. The patients were groupedaccording to 6 BMI groups: under-weight (BMI, <18.5), “normal”weight (BMI, 18.5-24.9), overweight(BMI, 25-29.9), class I obesity (BMI,30-34.9), class II obesity (BMI, 35-39.9), and class III obesity (BMI, ≥40).The incidence of major bleedingvaried significantly throughout theBMI spectrum: from underweight(5.6%) to normal-weight (2.5%) tooverweight (1.9%) to class I obese(1.6%) to class II obese (2.1%) to classIII obese (1.9%) patients (P<.001).Compared with normal-weightpatients, the risk of major bleedingwas higher in underweight patients(odds ratio, 2.29 [95% CI, 1.56-3.38])and lower in class I obese patients(odds ratio, 0.65 [95% CI, 0.47-0.90]).

HypertensionHypertension may increase

patients’ risk for a VASC develop-ing.3,12,37,74,79 In a study of 413 patientsundergoing PCI, it was reported thatpatients with a higher systolic bloodpressure (135 vs 129 mm Hg; df=410,P=.02) were significantly more likelyto have complications than werepatients with lower blood pressures.3

In a larger study of 13819 patients,Manoukian et al74 found that the644 patients (4.7%) who experiencedmajor bleeding were more likely tohave hypertension than were patientswithout major bleeding. Althoughelevated blood pressure during PCIand sheath removal may increasethe risk of VASCs, no evidence-basedblood pressure guidelines for PCIpatients are currently available.

Renal Dysfunction Renal dysfunction, defined as

creatinine clearance less than




60 mL/min,11 has been consistentlyidentified as a major risk factor forbleeding in patients undergoingPCI.11,12,37,74,76,81 The underlying mech-anism for such an association hasbeen postulated to be advanced age,as well as the presence of moresevere atherosclerosis and multiplecomorbid conditions.76 Patients withrenal dysfunction who are undergo-ing PCI are at increased risk of exces-sive dosing of anticoagulant andantiplatelet medications such as UFHand glycoprotein IIb/IIIa inhibitors,considering that most of these med-ications are eliminated via the kid-neys (Table 3).

Implications for NursingThe main goals of patient care

after PCI include maintenance ofhemostasis at the puncture site andassessment for VASCs. Achievingthese goals requires diligent assess-ment of patients with frequent mon-itoring of vital signs, puncture site,and pulse check. Duration of bedrest and time to ambulation dependon the method of arterial closureand the patient’s overall clinicalcondition. Figure 8 is an assessmentworksheet for units or individualnurses to use as a reference whengetting report from the catheteriza-tion laboratory or assessment checkson the unit. The worksheet assistsnurses in determining the patient’sbaseline assessment so that any

To learn more about percutaneous coro-nary intervention, read “Trait Anger, Hos-tility, Serum Homocysteine, and RecurrentCardiac Events After Percutaneous Coro-nary Interventions” by Song et al in theAmerican Journal of Critical Care, 2009;18:554-561. Available at www.ajcconline.org.

Figure 8 Worksheet to guide nurses in asking the right questions when gettingreport from the catheterization laboratory.

Sex __________

Age __________

Weight __________

BMI __________

Assessment of groin sites prior to procedure

Right Left

Palpable femoral pulse Y/N Palpable femoral pulse Y/N

Quality of pulse ___________ Quality of pulse _________

Bruit Y/N Bruit Y/N

Thrill Y/N Thrill Y/N

Assessment of dorsalis pedis and posterior tibial pulses

Right Left

Palpable dorsalis pedis pulse Y/N Palpable dorsalis pedis pulse Y/N

Quality of pulse _________ Quality of pulse ________

Dorsalis pedis pulse by Doppler Y/N Dorsalis pedis pulse by Doppler Y/N

Palpable posterior tibial pulse Y/N Palpable posterior tibial pulse Y/N

Quality of pulse _________ Quality of pulse _________

Posterior tibial pulse by Doppler Y/N Posterior tibial pulse by Doppler Y/N

Anticoagulant and/or antiplatelet used and dosage

Pre-procedure ____________

Intra-procedure ____________

Post-procedure ____________

Catheter size used ____________

Location of catheter ____________

High stick Y/N

Low stick Y/N

Hemostasis method ____________

Successful Y/N

Assessment of groin sites post-procedure

Right Left

Palpable femoral pulse Y/N Palpable femoral pulse Y/N

Quality of pulse ____________ Quality of pulse ____________

Bruit Y/N Bruit Y/N

Thrill Y/N Thrill Y/N

Assessment of dorsalis pedis pulse

Right Left

Quality of pulse Y/N Quality of pulse Y/N

Dorsalis pedis pulse by Doppler ________ Dorsalis pedis pulse by Doppler ________

Palpable posterior tibial pulse Y/N Palpable posterior tibial pulse Y/N

Quality of pulse ____________ Quality of pulse ____________

Posterior tibial pulse by Doppler Y/N Posterior tibial pulse by Doppler Y/N




procedural or medication-relatedcomplications can be promptly notedand addressed.

Never before has it been so clini-cally important to understand thepredictors and effect of VASCs inPCI, acute coronary syndrome, andSTEMI.37 Patients are increasinglytreated with higher complexity regi-mens containing greater numbersof more potent oral and intravenousantiplatelet and antithrombin med-ications for longer periods. Thesefactors can be expected to result inhigher rates of VASCs.35 Critically illpatients admitted to the intensivecare unit are at high risk for VASCsbecause of the presence of comorbidconditions such as renal failure,hypertension, and advanced age.These patients are also more likelyto be heavily anticoagulated and tohave had a high-risk, technicallydemanding procedure on an emer-gency basis.

Importantly, independent nursingjudgments regarding the methodsfor sheath removal and frequency ofmonitoring should be based on cur-rent evidence and knowledge of therisks for complications, given thepatient’s characteristics and the cir-cumstances surrounding the PCIprocedure. Nurses are in a goodposition to recognize VASCs whenthey occur and be knowledgeableabout management techniques toresolve them should they becomeproblematic. Understanding thatVASCs have both modifiable andnonmodifiable risk factors helpsnurses address issues that they canaffect while ensuring that at-riskpatients receive optimal monitoringand management. A thorough under-standing of vascular access issuesand prompt recognition of these

complications are essential to mini-mize the substantial morbidity,mortality, and hospital costs associ-ated with them. CCN

AcknowledgmentsEditorial assistance was provided by Rina Kleege,MS, of AdelphiEden Health Communications. Thisassistance was funded by Merck Sharp & DohmeCorp, a subsidiary of Merck & Co, Inc, White-house Station, New Jersey.

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CNE Test Test ID C1253: Managing Risk of Complications at Femoral Vascular Access Sites in Percutaneous Coronary InterventionLearning objectives: 1. Identify factors contributing to complications related to vascular access sites 2. Describe the different types of anticoagulation usedbefore, during, and after percutaneous coronary intervention 3. Define the methods of attaining hemostasis in patients undergoing percutaneous coronaryintervention

Program evaluation Yes No

Objective 1 was met ❑ ❑Objective 2 was met ❑ ❑Objective 3 was met ❑ ❑Content was relevant to my

nursing practice ❑ ❑My expectations were met ❑ ❑This method of CE is effective

for this content ❑ ❑The level of difficulty of this test was:

❑ easy ❑ medium ❑ difficultTo complete this program,

it took me hours/minutes.

1. Which of the following is the “gold standard” for achieving hemostasis atthe femoral access site after percutaneous coronary intervention (PCI)?a. Mechanical compression c. Manual pressureb. Vascular closure device d. Sand bag pressure

2. Which of the following is true regarding the use of low molecular weightheparin (LMWH) in PCI patients?a. LMWH has little effect on measurements of activated clotting time.b. LMWH is not as effective as unfractionated heparin and has a half-life 1 to 2 times longer than standard heparin. c. LMWH exerts its anticoagulant activity by deactivating antithrombin.d. Sheath removal followed by manual compression may be performed 6 hours after the last intravenous dose of LMWH.

3. Which of the following is true about direct thrombin inhibitors (DTIs)?a. DTIs inhibit thrombin-activated conversion of fibrinogen to fibrin.b. DTIs interact directly with thrombin molecules without the need for a cofactor.c. DTIs activate antithrombin, which plays a role in restricting thrombus formation.d. DTIs inhibit the cyclo-oxygenase enzyme, which stops prostaglandin synthesis and release.

4. Which of the following is true about clopidogrel?a. Clopidogrel resistance can occur in up to 30% of patients.b. Clopidogrel is a third-generation rapid-acting thienopyridine.c. The American College of Cardiology supports early administration of clopidogrel before catheterization for patients with unstable angina.d. Clopidogrel is an oral antiplatelet agent that prevents the final pathway of platelet aggregation by attaching to fibrinogen and other proteins, blocking platelet aggregation.

5. Femoral vascular access sites (VASCs) are often associated with all the following except which one?a. High femoral sticksb. Number of attempts c. Catheter sized. Use of contrast media during the procedure

6. Which of the following hemostasis methods does not allow the patient toget out of bed and ambulate faster?a. Suture mediated closure c. Extravascular clipsb. Collagen plug d. FemStop

7. Which of the following is not a nonmodifiable risk factor?a. Low body mass index (BMI) c. Advanced ageb. Hypertension d. Ethnicity

8. Which of the following is true regarding manual compression for obtaininghemostasis at the vascular access site?a. Hemostasis is achieved by placing the ring and middle fingers 2 to 4 cm below the access site. b. Hemostasis is achieved by applying pressure to the site immediately after the sheath has been removed.c. Manual compression requires firm compression for 15 to 20 minutes. d. Hemostasis is achieved by compressing the femoral artery against the femoral neck.

9. Which of the follow is true regarding the risk of VASCs in obese patients?a. Obese patients have a longer length of stay than patients with normal BMI.b. Obese patients are typically 6 years younger than patients undergoing PCI with

normal BMI.c. Obesity can decrease platelet aggregation.d. Obese patients have a greater risk of VASCs than patients with normal BMI.

10. Key implications for nursing care of patients after PCI include which of the following?a. Maintenance of hemostasis at the puncture siteb. Assessment for VASCsc. Assessment of the patient’s risk factors for VASCs including modifiable and nonmodifiable risksd. All of the above

11. Which of the following is the reported incidence of VASCs during PCI?a. 20%-30%b. 2%-15%c. 5.4%-20%d. 0%-40%

12. Low percutaneos entry through the femoral artery and vein approach for PCIcan predispose the patient to which of the following?a. Retroperitoneal hemorrhage of the inferior epigastric areab. Accidental puncture of another arteryc. Pseudoaneurysm, hematoma, and arteriovenous fistulad. Inguinal ligament injury

13. The American College of Cardiology Foundation/American Heart Associ-aiong/Society of Cardiovascular Angiography and Interventions support earlyadministration of which medication for patients at high risk for thromoboticevents related to bleeding?a. Prasugrelb. Aspirinc. Glycoprotein IIb/IIIAd. Unfractionated heparin

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Nakia Merriweather and Linda M. Sulzbach-HokeCoronary InterventionManaging Risk of Complications at Femoral Vascular Access Sites in Percutaneous

http://ccn.aacnjournals.org/Published online ©2012 American Association of Critical-Care Nurses

10.4037/ccn2012123 16-29 32 2012;Crit Care Nurse

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