Management of Access Site and Systemic Complications of Percutaneous Coronary and Peripheral Interventions

Abstract: The role of endovascular therapy for the treatment of coronary and peripheral vascular diseases (including carotid, renal and lower extremity arteries) is expanding. The steady growth in the volume of endovascular procedures is likely to result in an absolute increase in the incidence of procedural complications. Knowledge of common and specific procedural complications and their management are critical to successful outcomes. Complications can be classified as (i) access site-related and (ii) systemic. Reprinted with permission from The Journal of Invasive Cardiology 2008;20:463–469 The role of endovascular therapy for the treatment of coronary and peripheral vascular diseases (including carotid, renal and lower extremity arteries) is expanding. Knowledge of common and specific procedural complications and their management are critical to successful outcomes. Complications can be classified as (i) access site related and (ii) systemic. 1. Access Site-Related Complications A. Pseudoaneurysm A pseudoaneurysm (PSA) is defined as an arterial rupture of one or more layers of its walls, contained by overlying fibromuscular tissue, which communicates with an artery by a neck or sinus tract1 (Figure 1). Pseudoaneurysms occur in up to 7.5% of femoral artery catheterizations and can result in distal embolization, extrinsic compression on neurovascular structures, rupture and hemorrhage.2 Clinically the patient may complain of pain in the groin. A pulsatile groin mass with or without an audible bruit may be present on physical examination. Duplex ultrasound may provide evidence of extra-arterial flow or there may be classic “to-and-fro” Doppler waveform in the neck of the PSA (Figure 1). Before 1985, the treatment of PSA was surgical repair.3 Reports of the natural history of unrepaired PSA indicate that spontaneous closure can occur, especially with small PSAs. Large PSA (> 3 cm) that are symptomatic, expanding or those associated with large hematomas are generally thought the most prone to rupture.2,4 Ultrasound-guided compression was the treatment of choice for PSA in the 1990s.5,6 The procedure is successful in up to 90% of cases. Although the procedure is noninvasive, it has many disadvantages including prolonged compression time (up to 120 minutes), patient discomfort, early recurrence of PSA and limited success in treating large PSA.6,7 Ultrasound-guided thrombin injection for PSA of the iliac, femoral and peroneal arteries was pioneered by Cope and Zeit.8,9 Thrombin injection is safe, effective, associated with few complications and has emerged as the preferred treatment modality for pseudoaneurysms occurring as a result of percutaneous femoral arterial interventions.10,11 The procedure should be carried out by a physician with an ultrasonographer to enable continuous visualization of the PSA. Thrombin is introduced into the sac of the PSA away from the neck under direct ultrasound guidance (Figure 1). Small aliquot is given at a time and monitored for abolishment of spontaneous flow.12,13 Based on results from animal studies14,15 and indeed injecting of esophageal and gastric varices,16 thrombin injection of 0.5–2 ml at 1000 U/ml is considered a safe and effective dose range for PSA.17 A recent study of 274 patients with iatrogenic femoral PSA post-catheterization demonstrated ultrasound-guided thrombin injection was successful in 97% of cases.11 Complex PSA may require more than one injection of thrombin.18 Mohler et al have shown that the preferred approach for treating a PSA with multiple sacs is initial injection of the sac closest to the skin followed by injections of the deeper sacs.19 Potential complications of thrombin injection include leakage of thrombin causing thrombosis of the femoral artery and distal embolization.20 Contraindication for thrombin injection includes PSA with a wide, short neck, and associated arteriovenous fistula. B. Access site vessel occlusion In the event of acute vessel occlusion, the patient may complain of pain, pallor, parenthesis or decreased movement in the respective limb. Clinical examination may reveal a cold ischemic limb with absent pulses. An ankle-brachial index (ABI) 25% above baseline or > 0.5 mg/dl within 48 hours after radiocontrast media administration.49–52 Factors that have been identified to be associated with the development of CIN include: preexisting renal impairment, diabetes mellitus, advanced age, periprocedural intravascular depletion, congestive heart failure, volume and type of contrast administered, and concomitant use of other nephrotoxic drugs.53–55 The impairment tends to be non-oliguric and transient, with the peak serum creatine usually occurring around day 3 and returning to normal in the majority of cases within 2 weeks. Some patients may develop more severe renal failure, with approximately 1% of this group requiring dialysis. Although small in number, the morbidity and mortality rates in this group are alarmingly high, with an in-hospital mortality rate of up to 30% and an 80% 2-year mortality rate.55 The impairment of renal function after radiocontrast media exposure is multifactorial. Two predominant pathophysiological mechanisms proposed include contrast induced direct cytotoxic effects and vasoconstriction followed by either regional hypoxic damage or ischemia/reperfusion injury.56 Hydration as a prophylactic measure has a beneficial effect especially if the fluid load is given before the procedure.57 There are currently no studies of the optimal rate of prehydration, but most of the studies used a rate of 1–2 ml/kg/hr, for 6–12 hours preprocedure. Prehydration with normal saline has also been shown to be better than 0.45% saline, especially in women, diabetics, and patients receiving 250 ml or more of contrast.58 The use of isotonic sodium bicarbonate as a preventative measure for CIN has also been questioned and recent studies have suggested that bicarbonate alone may be associated with an increased risk of CIN.59 N-Acetylcysteine is the acetylated form of the amino acid L-cysteine and has long been established clinically as a mucolytic and as a treatment for acetaminophen overdose. Having antioxidant properties combined with a vasodilatory effect on the renal medullary circulation has led to studies evaluating its effects on CIN.60,61 Unfortunately no randomized trials exist but meta-analyses have shown that N-acetylcysteine significantly reduces the incidence of CIN, particularly when used with pre-hydration.61–63 A single trial has demonstrated significant beneficial effects from the use of another antioxidant, ascorbic acid, in patients with renal insufficiency undergoing coronary angiography.64,65 Other agents including adenosine antagonists,65 calcium channel antagonists,66 dopamine67 and fenoldopam68 in preventing CIN have all yielded equivocal results. The specific contrast agent used is also of importance in catheterization studies. Numerous studies, including a meta-analysis of 31 trials, have shown low-osmolar contrast media (LOCM) to be associated with significantly less CIN than high-osmolar contrast media in patients with renal impairment and/or diabetes.2 There has been considerable refinement during the past decades from ionic high-osmolar, to nonionic low-osmolar, and finally to nonionic iso-osmolar contrast media (IOCM). In patients with diabetes and/or chronic kidney disease, studies have shown that there may be a decrease in the postprocedural rise in creatine with the use of the iso-osmolar agent iodixanol compared to LOCM.69–71 However, it is unclear if this benefit translates into clinical outcomes, such as rehospitalization for renal failure or requiring hemodialysis, which actually favored the use of LOCM from registry data.72,73 Basic prophylactic measures include identifying those patients at risk, performing preprocedure assessment with a focus on volume status, identifying and withholding potentially nephrotoxic agents and drugs that may accumulate with reduced renal function such as aminoglycosides, nonsteroidal anti-inflammatory drugs (NSAID), metformin and digoxin. C. Acute stroke following cardiac catheterization Although strokes after cardiac catheterization are relatively rare, reported rates including both ischemic and hemorrhagic subtypes, range widely from 0.07% to 7.0%. Large contemporary registries of exclusively diagnostic and invasive coronary procedures report rates from 0.07% to 0.38%, and smaller studies of other invasive studies have reported higher rates.74 The etiology of ischemic stroke in this context can be dislodged aortic arch plaque which is calcified and fibrin-dense and therefore not amenable to lysis. Alternatively, calcific thrombi might partially lyse, leading to downstream emboli.75 Recent studies have shown a statistically and clinically significant early improvement in stroke severity in NIHSS score by 24 hours and indeed similar improvements were observed from baseline to 7 days in patients with acute stroke after cardiac catheterization treated with early thrombolysis.76 Low rates of intracranial and systemic hemorrhage were also noted in this study. Future large, prospective registries to further characterize this population are needed. Conclusion The steady growth in the volume of endovascular procedures is likely to result in an absolute increase in the incidence of procedural complications. Competent operators must have a broad knowledge of potential systemic and vascular access complications as well as an understanding of the management of these complications (Table 1).

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