Manual Compression May Not Be Benign!
An endovascular surgeon’s “view from the inside” of vascular access site hemostasis.
To view the figures and tables related to this article, please refer to the print version of our April issue, page 42.
In 1953, Seldinger classically reported the original description of percutaneous femoral artery access, and in so doing, first reported vascular access hemostasis (VAH).1 Since then, significant technological advances in the field of catheter-based cardiovascular therapy have rendered most early percutaneous technology obsolete. It is remarkable that 50 years later, the gold standard of VAH remains manual compression (MC), performed almost exactly as Seldinger originally described: “20-30 minutes hand-held pressure after catheter removal followed by overnight bed rest.”1
MANUAL COMPRESSION—THE GOLD STANDARD?
This gold standard remained largely unchallenged over the next 4 decades, until the widespread adoption of percutaneous cardiovascular interventions. These procedures require larger sheaths and more potent anticoagulation. Multiple percutaneous coronary intervention (PCI) trials drew attention to ischemic and hemorrhagic complications helping to spawn the development of vascular closure devices (VCD). VCDs are designed to facilitate hemostasis, ambulation, and hospital discharge without increasing complications.2-8 In reporting the recent results of the Suture To Ambulate and Discharge (STAND I and STAND II) trial, Baim et al7 noted, “despite advances in other aspects of cardiac catheterization, manual compression followed by 4 to 8 hours of bed rest remains the mainstay (gold standard) of postprocedural femoral access site management.” VCD trials also use MC as their gold standard for comparison of outcomes and this gold standard designation seems to be substantiated in a recent editorial comment by Tarvis et al10 in Arteriotomy Closure Devices – The FDA Perspective. These VCD trials have also created an opportunity for critical review of the literature and closer scrutiny of MC in VAH.
THE PROBLEM EXPOSED
Femoral artery access complications (FAC) remain a significant source of mortality and are the leading cause of morbidity after PCI.8-11 Remarkably, no standardization exists in regard to reporting “major” and/or “minor” FAC rates, which vary widely from 0.4% to 27% depending upon the definition of complications. 7-9,12 Most reports cite only “major” FACs requiring surgery, and it is highly likely that many FACs go unreported or are accepted as part of the territory. Popma et al 11 were among the first to identify FACs as a major problem noting a 14% bleeding rate with PCI. In a randomized trial comparing MC to AngioSeal (St. Jude Medical, St. Paul, MN), Kussmall et al8 reported a 27% overall “any complication” rate in the MC group with heparin. In 2001, Danges et al9 compared MC (N = 4,596) to VCDs (N = 497) after PCI and reported higher “overall complication” rates with VCDs versus MC (21.4% versus 12.1%, respectively), again confirming significant “overall complications” with MC and identifying that current VCD use may increase complications.
Pracyk et al13 cited a 64% overall FAC rate with MC when patients were thoroughly scrutinized by physical examination and duplex ultrasound. A review of the literature reveals sparse data on MC in regard to a hemostatic mechanism, healing or scarring of the arteriotomy site, short- or long-term femoral artery (FA) clinical sequale, systemic effects of a groin hematoma, or a consensus recommendation on the safety, risks, and timing of FA reentry. After 50 years of truly remarkable cardiovascular technological achievements, it seems reasonable to ask the questions, “Why?” and “Should MC still be the gold standard?”
AAA EVS: AN OPPORTUNITY TO EXPOSE
Simultaneous with the development of VCDs, endovascular stentgraft (EVS) exclusion for abdominal aortic aneurysms (AAA) became approved, requiring FA surgical exposures and presenting a unique opportunity to grossly study the FA after diagnostic angiography where VAH was achieved with MC or a VCD. Between 1999 and 2002, 105 FAs were electively exposed for AAA EVS and over 4,000 intraoperative photos taken evaluating the FA from 1 to 30 days after angiography. A FA perivascular scar score (PSS) was developed to objectively analyze the FA with VAH provided by MC (N=55) and VCD (N=50); [VCD = suture mediated closure (SMC) = 38; syvek thrombotic patch (Marine Polymer Technologies, Danvers, MA) (STP) = 10; and a novel staple closure device = 2 (Angiolink, Angiolink Corporation, Taunton, MA)]. All patients had 6F diagnostic angiography with a single bolus of heparin (3,000 IU). MC was performed using standard two-hand pressure placed 1.0 cm above and 1.0 cm below the FA for 30 minutes, followed by 4 hours of bed rest and ambulation and discharge when stable. SMC was performed with the Perclose-S device (Abbott Laboratories, Abbott Park, IL). The technique used for SMC and STP was as described in the device insert. The time to surgery (TTS) was defined as the time between angiography to surgery.
THE PERIVASCULAR SCAR SCORE
The PSS was assigned and recorded for each FA after analysis of photos immediately at the termination of surgery by the same operator (DEA). No FAs were considered normal after angiography. A PSS was assigned as mild = 1, moderate = 2, and severe = 3 (Figure 2) (Table 1). The PSS results are summarized in Table 2.
PSS Results Raise Clinical Questions
There have been no previous reports attempting subjective or objective evaluation of FA morphology after the use of MC or VCDs. Predictably, each VAH technique resulted in vascular and perivascular scarring, but key unsuspected findings include: (1) For all closure techniques, PSS was >2.50; therefore, all resulted in significant FA morphologic changes. The MC PSS was worse than that of SMC or STP, but not statistically significant. (2) Morphologic findings occurred even 2 weeks (mean, 12.5 to 14 days) after VAH, raising many questions regarding the timing, safety, and appropriateness of FA reaccess and the short- and long-term FA clinical sequelae associated with MC and VAH (Figures 3 and 4).
FACs—CLINICAL AND ECONOMIC COSTS
Aguirre et al14 found FAC increased the length of patient stay to an average of 3.5 days compared to <2 days in an uncomplicated PCI. Moscucci et al15 has suggested that FAC may indirectly increase ischemic complications after PCI when they reported the incidence of death and myocardial infarction (MI) among patients with FAC as 2.4% and 13% respectively, versus 0.2% and 3.0% in 4,090 PCI patients without FAC (P <0.0001).16 Extrapolating financial costs to FAC is difficult, but in tracking blood transfusions after PCI, Lauer et al has estimated a single unit of blood transfusion during PCI to add an additional $8,000 to the overall cost of that hospitalization.16,17
GOLD STANDARD CLINICAL LIMITATIONS
Reported major FACs associated with MC include active or late FA bleeding requiring surgery, pseudoaneurysm, A-V fistula, retroperitoneal hematoma, large (>5.0 cm) hematoma, requirement of 2 u blood transfusion, secondarily infected hematoma, and FA and femoral venous thrombosis.8,11 Reported minor FAC with MC include small (<5.0 cm) nonsurgical hematoma, <2 u blood transfusion, periprocedural and prolonged leg pain, leg weakness and numbness, prolonged oozing, ecchymosis, bruit, acute and prolonged painful mass, back pain, prolonged immobilization, increased length of stay, increased resource utilization, and increased costs.8,11 Multiple patient-satisfaction surveys have consistently identified the importance of patient comfort, ease in ambulation, and need to “improve the overall interventional experience,” but this remains a low priority in healthcare.18-20 Ricckli et al21 reported 76% of patients who experienced both MC and VCDs would prefer VCDs for future VAH, further identifying this under appreciated limitation of MC (VCD with earlier MC or vice versa).
Less obvious but potentially significant clinical limitations of MC may include:
(1) VAH with MC often requires cessation or interruption of therapy because MC requires temporarily stopping anticoagulation (heparin, lytic agents, GP IIb/IIIa’s, etc.) and allowing activated clotting time (ACT) levels to return to <150 to 180 seconds to achieve VAH. This may have significant thrombotic or ischemic clinical consequences in patients requiring complex PCI or infrainguinal revascularization in which prolonged periprocedural anticoagulation may be clinically desirable. VAH management with a VCD could allow immediate sheath removal without stopping anticoagulation or lysis, neither of which are possible with MC.
(2) MC reduces FA blood flow simultaneous with a return to a normal thrombotic state as the ACT normalizes. This could potentially provoke subacute thrombosis of a successfully stented vessel, especially in the treatment of ipsilateral iliofemoral, popliteal, or infrapopliteal disease.
(3) Most data on FAC is extrapolated from PCI trials, not percutaneous peripheral interventional (PPI) trials. PCI trials use smaller sheaths (5F to 6F) than those routinely used for PPI (7F to 8F). Larger sheath size, anticoagulation, PVD, and complex interventions have consistently been predictors for bleeding and are commonly associated with PPI. Therefore, it seems reasonable to assume that MC FAC would be reported more often with PPI than PCI underscoring the importance of an “ideal VCD,” especially in the PPI treatment of PVD.
(4) An extensive review of the literature reveals no published guidelines or recommendations on the timing, technique, or risks of FA re-entry after MC, and clinical opinions on timing vary from immediate to several weeks postprocedure. In our study, all FAs exposed less than 7 days after MC revealed that the vessel wall appeared grossly weakened by extensive intramural ecchymosis and hematoma. The arteriotomy site also appeared unhealed and contained a tenuous “platelet plug” (Figure 4). This gross appearance of the FA should at least raise questions regarding FA reaccess and calls for evidence-based recommendations regarding the timing and safety of FA reentry. Reentry soon after MC may not be benign.
(5) Although the use of protamine reversal is less common today, severe allergic reactions can be associated with significant morbidity, and complete protamine avoidance would be clinically desirable.22,23 Immediate, secure, safe VAH with a VCD would obviate any need for protamine.
A NEW GOLD STANDARD—THE IDEAL VCD
Certainly the results of the PSS lack the scientific evidenced basis to definitively challenge MC as the gold standard of VAH. This analysis may even raise more questions than answers, but a critical review of the literature and a look at our own clinical practices will reveal that access site complications are much more than just a nusiance, they are major clinical problem. After 50 years, it is time to question the gold standard for VAH and challenge clinicians and industry to develop a simple, safe, immediately effective, secure, reliable, cost-effective, complication-free VCD that allows safe continuation of anticoagulation and almost immediate FA reaccess that is universally applicable for all catheter-based procedures, the “ideal VCD.”
The potential clinical opportunity for the ideal VCD would be every diagnostic and interventional procedure performed in every radiology suite, catheterization laboratory, or endovascular suite worldwide. When the ideal VCD is available there would be no reason not to use it on every procedure because patients will want it and healthcare will need it. The ideal VCD could change the primary goal of VCD VAH management from one of “primarily convenience” to a theme of “primary treatment,” as the ideal VCD should be a part of the treatment planning and strategy for each patient.
David E. Allie, MD, is Director of Cardiothoracic and Endovascular Surgery at the Cardiovascular Institute of the South in Lafayette, Louisiana. He is a member of the Angiolink Scientific Advisory Board and a physican VCD trainer for Abbott Laboratories. Dr. Allie may be reached at (800) 582-2435; David.Allie@cardio.com.
Chris J. Hebert, RT, RCIS, is Director of Technology at the Cardiovascular Institute of the South in Lafayette, Louisiana. He is a a physican VCD trainer for Abbott Laboratories and a research consultant for Angiolink Corporation. Mr. Hebert may be reached at (800) 582-2435; Chris.Hebert@cardio.com.
Craig M. Walker, MD, is Medical Director of the Cardiovascular Institute of the South in Houma, Louisiana. He is a member of the Angiolink Scientific Advisory Board and a physican VCD trainer for Abbott Laboratories. Dr. Walker may be reached at (800) 445-9676; Craig.Walker@cardio.com.
Ronald P. Caputo, MD, heads S.J.H. Cardiac Catheterization Associates in Syracuse, New York. He is Chairman and Chief Medical Officer of Angiolink Corporation. Dr. Caputo may be reached at (315) 448-6215; email@example.com.
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