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Indications & Contraindications
Rutherford classification, patient selection, CLI criteria
Indications
- Lifestyle-limiting claudication (Rutherford 2–3) — failed conservative management (exercise therapy, cilostazol ≥3 months)
- Critical limb ischemia (CLI) — rest pain (Rutherford 4), minor tissue loss / non-healing ulcer (Rutherford 5), major tissue loss / gangrene (Rutherford 6)
- ABI <0.9 diagnostic for PAD; ABI <0.4 or absolute ankle pressure <50 mmHg suggests CLI
- Hemodynamically significant stenosis (≥50% with pressure gradient) or occlusion confirmed on imaging
- Acute limb ischemia (ALI) with viable or marginally threatened limb (Rutherford I–IIa)
Contraindications
- Uncorrectable coagulopathy — active bleeding diathesis
- No viable target limb — irreversible ischemia, extensive gangrene requiring primary amputation
- Severe contrast allergy without premedication
- Severe renal insufficiency (relative) — consider CO2 angiography or minimal contrast technique
- Relative: heavily calcified non-dilatable lesion (consider atherectomy first)
- Relative: target artery <2 mm diameter (limited device options)
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Pre-Procedure Planning
Imaging workup, labs, antiplatelet management, consent
Imaging Workup
- ABI / TBI: baseline measurement; TBI preferred if ABI falsely elevated (>1.3) due to calcified vessels (diabetes, ESRD)
- Duplex ultrasound: first-line; identifies stenosis location, peak systolic velocity ratios (>2.5 = ≥50% stenosis)
- CTA runoff: aorta to feet; defines lesion length, calcification burden, runoff vessels; essential for procedure planning
- Catheter angiography: gold standard; often combined with same-session intervention; includes pressure gradient measurement across lesions
- MRA (if CTA contraindicated due to renal insufficiency or allergy) — may overestimate stenosis at calcified segments
Labs & Medications
- CBC, BMP (creatinine/eGFR), PT/INR, PTT
- Type & screen for complex cases or anticipated large-bore access
- Antiplatelet management: aspirin 81–325 mg daily continued; clopidogrel 75 mg loaded pre-procedure if stent anticipated
- Post-stent DAPT: aspirin + clopidogrel × 1–3 months minimum (longer for DES/covered stents)
- Hold metformin if contrast load anticipated with borderline renal function
- IV hydration protocol for CKD patients (NS 1 mL/kg/h × 12h pre & post)
Non-invasive vascular lab completed. ABI/TBI and segmental pressures documented; duplex US reviewed.
CTA runoff reviewed. Lesion location, length, calcification burden, and runoff vessels assessed. TASC classification assigned for aortoiliac and femoropopliteal disease.
Antiplatelet therapy confirmed. Aspirin continued; clopidogrel loaded (300–600 mg) if stent planned. DAPT regimen documented.
Labs reviewed. Creatinine/eGFR acceptable for contrast; coagulation parameters within range; CBC stable.
Consent obtained. Key risks discussed: bleeding/hematoma, pseudoaneurysm, dissection, distal embolization, vessel perforation, contrast nephropathy, stent thrombosis/fracture, limb loss (rare).
Access site planned. CFA antegrade, retrograde, or contralateral approach selected based on lesion location and patient anatomy.
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Relevant Anatomy
Aortoiliac, femoropopliteal, infrapopliteal segments; TASC classification; angiosomes
Aortoiliac Segment
- Infrarenal aorta → common iliac arteries → bifurcation into external and internal iliac arteries
- External iliac → becomes CFA at inguinal ligament
- TASC A: single short (≤3 cm) CIA or EIA stenosis (endovascular first)
- TASC B: short (≤3 cm) aortic stenosis, unilateral CIA occlusion, single/multiple EIA stenoses 3–10 cm
- TASC C: bilateral CIA occlusions, bilateral EIA stenoses, unilateral EIA stenosis involving CFA origin
- TASC D: infrarenal aortobiiliac occlusion, diffuse bilateral disease — historically surgical, but endovascular increasingly performed
Femoropopliteal Segment
- CFA bifurcates into SFA (anterolateral) and profunda femoris (posterolateral)
- SFA courses anteromedially through the thigh in the adductor canal (Hunter canal)
- Adductor hiatus: SFA exits the adductor canal to become popliteal artery — high mechanical stress zone, common site for restenosis and stent fracture
- Popliteal artery: from adductor hiatus to trifurcation below the knee
- SFA is the most commonly diseased segment in PAD; long lesions and chronic total occlusions (CTOs) are frequent
Infrapopliteal Segment
- Tibial trifurcation: popliteal artery divides into anterior tibial (AT), tibioperoneal trunk → posterior tibial (PT) + peroneal arteries
- AT: crosses interosseous membrane anteriorly; becomes dorsalis pedis artery
- PT: courses posterior in deep calf; runs behind medial malleolus; supplies plantar arch
- Peroneal: runs along fibula; terminates as lateral calcaneal branches; does not directly reach foot (communicates via collaterals)
- Angiosomes: foot divided into 6 territories fed by specific source arteries; angiosome-directed revascularization in CLI improves wound healing
Angiosome Map (Key Territories)
| Angiosome | Source Artery | Clinical Relevance |
|---|---|---|
| Dorsal foot | Dorsalis pedis (from AT) | Dorsal foot wounds; toe amputations |
| Plantar heel | Calcaneal branch of PT | Heel ulcers — most common CLI wound location |
| Medial plantar | Medial plantar (from PT) | Medial midfoot wounds |
| Lateral plantar | Lateral plantar (from PT) | Lateral forefoot / 5th metatarsal wounds |
| Lateral ankle / heel | Peroneal (calcaneal branches) | Lateral malleolar ulcers |
| Medial ankle | PT (malleolar branches) | Medial malleolar ulcers |
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Technique
Access, wire traversal, angioplasty, stenting, atherectomy
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Arterial Access
Contralateral CFA access: standard starting point — retrograde micropuncture under US guidance over medial femoral head; up-and-over technique into ipsilateral iliac/femoral system. Ipsilateral antegrade CFA: preferred for ipsilateral SFA/popliteal/tibial lesions; skin entry 2–3 cm above CFA to allow sheath angulation. Radial artery (right): increasingly favored for patients with bilateral groin disease, post-femoral bypass, morbid obesity, or aortoiliac occlusion — use 6F radial sheath with 90–110 cm Destination or Flexor Raabe long sheath; permits treatment of infrarenal aortoiliac and femoropopliteal disease; TR Band for hemostasis. Avoid >6F through radial. Pedal access: retrograde tibial or pedal artery puncture for CTO crossing when antegrade approach fails (SAFARI technique). Heparin 50–70 U/kg IV bolus after sheath placement; target ACT 250–300 sec.
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Diagnostic Angiography
Perform complete runoff angiography from aortic bifurcation to pedal arch. Assess inflow (iliac), target lesion, and runoff vessels. Measure pressure gradients across lesions (systolic gradient >10 mmHg at rest or >15 mmHg with vasodilator = hemodynamically significant). Identify collateral pathways. Plan intervention based on lesion characteristics: length, calcification, degree of stenosis vs occlusion.
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Lesion Crossing
Intraluminal crossing: preferred for stenoses and short occlusions; use hydrophilic guidewire (0.035" Glidewire or 0.014" for tibials) with support catheter. Subintimal crossing: intentional entry into subintimal plane for long CTOs; wire re-enters true lumen distally; use re-entry devices (Outback, Pioneer) if needed. Subintimal dissection plane typically easier in calcified CTOs. Confirm true lumen re-entry with contrast injection before intervention.
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Balloon Angioplasty (PTA)
Plain balloon angioplasty: first-line for most lesions; balloon sized 1:1 to reference vessel diameter; inflation 2–3 minutes. Drug-coated balloon (DCB): preferred over BMS in the SFA — paclitaxel-coated balloons (IN.PACT Admiral, Lutonix) reduce restenosis; inflate ≥2 minutes for adequate drug transfer. Below-knee PTA: standard therapy for infrapopliteal disease in CLI; long inflation times (3–5 minutes); sized 1:1 or slightly undersized to reference vessel.
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Stenting
Bare-metal stents (BMS): self-expanding nitinol stents for iliac and SFA/popliteal disease; used for flow-limiting dissection, residual stenosis >30%, or elastic recoil after PTA. Drug-eluting stents (DES): paclitaxel-coated (Zilver PTX) shown to reduce restenosis in SFA compared to BMS. Covered stent-grafts: Viabahn for long SFA lesions, vessel perforations, or as salvage for failed PTA/stenting. Balloon-expandable stents: reserved for aortic bifurcation (kissing stents) and ostial common iliac lesions where precise placement and radial strength are critical.
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Atherectomy
Directional atherectomy (SilverHawk, TurboHawk): excises plaque; useful for focal calcified lesions; often combined with DCB. Orbital atherectomy (Diamondback 360): sands calcified plaque; useful for heavily calcified infrapopliteal lesions. Laser atherectomy (Excimer laser): photoablation; useful for in-stent restenosis. Atherectomy serves as vessel preparation before balloon angioplasty or DCB; use with distal embolic protection device (Spider, Emboshield) when possible.
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Completion Angiography & Closure
Completion angiography to confirm <30% residual stenosis, no flow-limiting dissection, and adequate runoff to foot. Assess pedal arch reconstitution in CLI cases. Remove sheath; achieve hemostasis with manual compression (15–20 min) or vascular closure device (Angio-Seal, Perclose, Mynx). If antegrade puncture: manual compression preferred. Post-procedure ABI/PVR at bedside to confirm hemodynamic improvement.
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Key Landmarks
CFA puncture site, SFA origin, adductor hiatus, tibial trifurcation
CFA Puncture Site
- CFA overlies the medial third of the femoral head on fluoroscopy — optimal puncture target
- Below the inguinal ligament (midpoint between ASIS and pubic tubercle)
- Puncture above the inguinal ligament risks retroperitoneal hemorrhage (no compression against bone)
- Puncture at or below the CFA bifurcation increases risk of pseudoaneurysm, AVF, and limits closure device use
- US-guided access improves first-pass success and reduces complications — strongly preferred
Critical Transition Zones
- SFA origin: arises anterolaterally; profunda femoris arises posterolaterally ~1–2 cm below the inguinal ligament — preserve profunda at all costs (critical collateral source)
- Adductor hiatus: SFA transitions to popliteal artery at the adductor (Hunter) canal; zone of high mechanical stress from knee flexion; avoid stenting across this zone when possible (fracture risk)
- Tibial trifurcation: popliteal artery divides below the knee joint line; AT passes anterior through interosseous membrane; tibioperoneal trunk continues 2–3 cm then divides into PT and peroneal
- Pedal arch: dorsalis pedis (from AT) connects with lateral plantar (from PT) to form plantar arch; intact arch = better CLI outcomes
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Troubleshooting
CTO crossing, dissection, embolization, perforation, access issues
CTO Crossing Failure
Unable to Cross Chronic Total Occlusion with Guidewire
Attempt intraluminal crossing first with stiff hydrophilic wire and support catheter. If unsuccessful, intentional subintimal crossing with a looped Glidewire or CTO-specific wire (Astato, Confianza). For long CTOs, consider retrograde pedal access (SAFARI technique) with rendezvous in the CTO body. Re-entry devices (Outback catheter) to return from subintimal plane to true lumen. If all endovascular approaches fail, consider surgical bypass referral.
Dissection
Flow-Limiting Dissection After Angioplasty
Mild non-flow-limiting dissections are common and often resolve spontaneously. For flow-limiting dissections (reduced antegrade flow, intimal flap obstructing >50% lumen): place self-expanding stent across the dissection to tack down the flap. Covered stent-graft (Viabahn) for extensive or spiral dissections. Prolonged balloon inflation (3–5 min, low atmosphere) may seal minor dissections without stent placement. Always confirm restored flow on completion angiography.
Distal Embolization
Acute Loss of Runoff Vessels During Intervention
Immediate recognition: loss of previously patent tibial vessels on angiography, new filling defects. Aspiration thrombectomy: advance aspiration catheter (Penumbra, Export) to embolus and aspirate. Mechanical thrombectomy: AngioJet rheolytic thrombectomy for larger thrombus burden. Catheter-directed TPA (2–4 mg alteplase bolus into affected vessel) for small distal emboli. Prevention: use embolic protection devices during atherectomy; consider prophylactic heparin dose check (ACT >250).
Vessel Perforation
Contrast Extravasation During or After Intervention
Immediately inflate balloon across the perforation site to achieve tamponade (low-pressure, prolonged inflation 5–10 min). If balloon tamponade fails or perforation is large: place covered stent-graft (Viabahn or iCast) across the perforation. For small tibial perforations: prolonged balloon inflation usually sufficient; coil embolization as salvage if there is adequate distal collateral flow. Reverse anticoagulation with protamine if ongoing hemorrhage. Monitor for compartment syndrome (calf swelling, pain with passive stretch).
Access Site Complication
Hematoma, Pseudoaneurysm, or Retroperitoneal Hemorrhage
Hematoma: manual compression; if expanding, reverse anticoagulation. Pseudoaneurysm: US-guided thrombin injection (first-line for post-catheterization pseudoaneurysm >2 cm); US-guided compression if thrombin contraindicated. Retroperitoneal hemorrhage: suspect if high puncture above inguinal ligament with unexplained hypotension, back/flank pain; emergent CT; resuscitate aggressively; consider covered stent or surgical repair if hemodynamically unstable. Assess H/H serially.
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Complications
Procedural and post-procedural adverse events
Intraprocedural
- Dissection — most common; usually managed with stent placement; flow-limiting dissection requires immediate treatment
- Distal embolization — plaque or thrombus dislodgement; more common with atherectomy; use embolic protection when available
- Vessel perforation — wire or device-related; balloon tamponade first; covered stent if needed
- Access site hemorrhage — hematoma (5–10%), pseudoaneurysm (1–2%), retroperitoneal hemorrhage (<1%)
- Vessel spasm — especially tibial arteries; intraarterial nitroglycerin 100–200 mcg or verapamil 2.5 mg
Post-Procedural
- Contrast nephropathy — creatinine rise ≥0.5 mg/dL or ≥25% within 48–72h; hydration is best prevention; limit contrast volume
- Stent thrombosis — acute (<30 days) or subacute; ensure DAPT compliance; may require re-intervention
- Stent fracture — especially in SFA across adductor hiatus; associated with restenosis and re-occlusion
- Restenosis / re-occlusion — neointimal hyperplasia; 1-year primary patency: DCB ~80%, BMS ~65%, PTA alone ~50% (SFA)
- Limb loss — rare with elective procedures (<1%); higher risk with failed CLI revascularization
- Pseudoaneurysm — pulsatile mass at access site; diagnosed by US; treat with thrombin injection
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Pearls & Pitfalls
Clinical decision-making tips and common mistakes
✦
Treat inflow first. Always address iliac disease before treating SFA or tibial lesions. An SFA stent will fail quickly without adequate inflow. Iliac PTA/stenting has excellent long-term patency (>90% at 5 years) and improves outcomes of distal interventions.
✦
Angiosome-directed therapy for CLI. Revascularize the artery that directly supplies the wound territory. Direct revascularization of the appropriate angiosome in CLI patients significantly improves wound healing and limb salvage compared to indirect revascularization.
✦
DCB preferred over BMS in the SFA. Drug-coated balloons (IN.PACT Admiral, Lutonix) have shown superior patency rates compared to bare-metal stents in the SFA with the advantage of leaving nothing behind. Reserve stenting for bailout (dissection, recoil).
✦
Avoid stenting across the knee joint. Stents spanning the adductor hiatus and popliteal fossa are subject to repetitive flexion/extension forces, leading to high rates of stent fracture and restenosis. If stenting is required distally, stop above the joint line or use a covered stent-graft designed for this zone.
✦
Pedal loop reconstitution. In CLI, even if only one tibial vessel is patent, establishing inline flow to the pedal arch dramatically improves wound healing. The connection between the dorsalis pedis and plantar arch creates a loop that perfuses multiple angiosomes.
⚠
Do not neglect the profunda femoris. The profunda is the most important collateral pathway in SFA occlusive disease. Avoid covering or compromising the profunda origin when placing SFA stents. If profunda origin is diseased, treat it first.
⚠
Watch ACT and anticoagulation during long cases. Subtherapeutic heparinization during prolonged CTO crossing or multi-level intervention is a common cause of acute thrombotic occlusion. Re-bolus heparin to maintain ACT >250 sec; recheck ACT every 30–45 minutes.
⚠
Beware of reperfusion injury. After successful revascularization of a severely ischemic limb, monitor closely for compartment syndrome (pain out of proportion, swelling, pain with passive stretch). Early fasciotomy may be limb-saving.
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References & Resources
Primary sources, landmark trials, and related procedures
Landmark Trials
- IN.PACT Admiral (2015): DCB vs PTA in SFA — superior 12-month primary patency with paclitaxel DCB (82.2% vs 52.4%)
- Zilver PTX (2011): DES vs BMS/PTA in SFA — paclitaxel DES showed sustained patency benefit through 5 years
- TASC II (2007): Inter-society consensus classification for aortoiliac and femoropopliteal disease guiding endovascular vs surgical treatment selection
Primary References
- Norgren L, Hiatt WR, Dormandy JA, et al. Inter-Society Consensus for the Management of Peripheral Arterial Disease (TASC II). J Vasc Surg. 2007;45 Suppl S:S5–S67.
- Rosenfield K, Jaff MR, White CJ, et al. Trial of a paclitaxel-coated balloon for femoropopliteal artery disease (IN.PACT Admiral). N Engl J Med. 2015;373(2):145–153.
- Dake MD, Ansel GM, Jaff MR, et al. Paclitaxel-eluting stents show superiority to balloon angioplasty and bare metal stents in femoropopliteal disease: twelve-month Zilver PTX randomized study results. Circulation. 2011;124(18):1949–1956.
- Conte MS, Bradbury AW, Kolh P, et al. Global vascular guidelines on the management of chronic limb-threatening ischemia. J Vasc Surg. 2019;69(6S):3S–125S.e40.
- Gerhard-Herman MD, Gornik HL, Barrett C, et al. 2016 AHA/ACC Guideline on the Management of Patients with Lower Extremity Peripheral Artery Disease. Circulation. 2017;135(12):e726–e779.