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Complications - Endovascular Therapy of a Penetrating Atheromatous Aortic Ulcer of the Descending Aorta (PAU, TEVAR)

  1. Intraoperative Complications

    1. Complications of Access Routes

    • Frequency: 9-16 % of all patients
    • Injuries to access vessels with or without acute thrombosis, bleeding complications; later also pseudoaneurysm formation and arteriovenous fistulas
    • especially in narrow, delicate or highly tortuous, calcified vessels
    • Dissection, occlusion of the access vessel, vessel rupture → Stent implantation
    • Bleeding complication at puncture site (5-8 %) → mostly conservative; surgical hematoma evacuation with vessel suturing in < 3 % of cases required

    Prophylaxis:

    • careful patient selection and preprocedural evaluation
    • correct selection of the introducer set

    2. Misplacement of the Endoprosthesis

    too low placement:

    • inadequate proximal sealing → Endoleak Type I
    • proximal extension with additional stent graft or bare-metal stent

    too high placement:

    • interventional therapy is no longer possible (frequently) → conversion to open surgery 

    inadequate sealing of the PAU:

    • Endograft extension

    Endoleak:

    Modeling using balloon, if necessary central and/or peripheral extension

    Prophylaxis:

    • careful preprocedural evaluation
    • familiarize oneself with the various markings on the endograft
  2. Postoperative Complications

    1. Ischemic Complications

    Visceral Ischemia

    • due to malpositioning of the endograft covering the celiac trunk
    • Treatment: open removal of the endograft and, depending on the situation, open correction of the PAU

    Spinal Ischemia and Paraplegia (“ischemic spinal cord injury” – SCI)

    • Cause: Reduced blood flow to the spinal cord due to endovascular overstenting of spinal cord-relevant arteries in combination with other risk factors such as perioperative hypotension, larger blood losses/anemia; especially in thoracic/thoracoabdominal procedures
    K 328-1

    Territories of Spinal Cord Perfusion ("Collateral Network")

    supra-aortic

    cervical arteries (esp. vertebral artery)

    thoracic aorta

    intercostal arteries

    abdominal aorta

    lumbar arteries

    pelvic

    internal iliac artery

    If at least two territories of spinal perfusion are compromised, the likelihood of spinal ischemia increases.

    • Clinical presentation: ranges from small transient sensory impairments to functional disorders of continence organs to complete paraplegia with lifelong bedriddenness and need for care

    Mechanisms of Spinal Cord Ischemia

    Disorder

    Effect

    persistent clamping of the aorta

    acute loss of direct (spinal arteries) and indirect (collateral network) spinal cord perfusion

    decrease in mean arterial pressure (e.g., due to anesthesia)

    decrease in spinal perfusion pressure/acute hypoperfusion

    increasing pressure of cerebrospinal fluid

    spinal compartment syndrome

    steal phenomenon through open spinal arteries e.g. after opening an aneurysm sac

    decrease in spinal perfusion pressure -> spinal cord edema

    reperfusion injury after clamping

    spinal cord edema

    postoperative thrombosis of arteries supplying the spinal cord

    delayed paraplegia

    • Treatment:  Increase in spinal perfusion pressure, e.g. pharmacological elevation of mean arterial pressure and placement of a cerebrospinal fluid drain to reduce the counterpressure of arterial perfusion in the cerebrospinal fluid spaces

    Prophylaxis:

    • Avoid intra- and postoperative hypotensive phases and, after segmental artery occlusion, maintain a mean arterial pressure of 80–90 mm Hg for at least 48 h
    • Placement of a prophylactic spinal cerebrospinal fluid drain if at least two territories of spinal blood flow (see above) are impaired and cannot be reopened by revascularizing measures
    • perioperatively sufficient central venous saturation (ScvO2) of ≥70 % as well as intraoperatively a central venous pressure (CVP) of ≤10 mm Hg, hemoglobin value ≥ 8 mg/dl or keep intraoperative blood loss as low as possible, cell saver
    • postop. prompt extubation to assess neurological status, follow-up checks

    Limb Ischemia  

    • peripheral emboli (< 2 %) → resolution through combination of thrombolysis, catheter aspiration, angioplasty/stent as well as Fogarty maneuver

    2. Systemic Complications

    • cardiopulmonary and cerebrovascular complications as well as contrast-induced nephrotoxicity
    • acute coronary syndrome, myocardial infarction, pneumonia, cerebrovascular events, renal insufficiency → adequate, interdisciplinary treatment
    • preoperative evaluation: cardiac status, lung function, retention values

     3. Post-Implantation Syndrome

    • Incidence: 13 – 60 %
    • Cause: inflammatory immune response with release of cytokines due to endothelial activation by the endograft material
    • Clinical presentation: transient, acute, flu-like symptoms, fever
    • Laboratory: elevation of C-reactive protein (CRP), interleukin-6 and TNF-α during the first week after implantation; typically no leukocytosis and no pathogen detection
    • Treatment: symptomatic (antipyretic measures, antibiotics are not indicated)

    4. Pseudoaneurysms of Access Vessels 

    • at the puncture site after percutaneous approach more common than after surgical exposure of the access vessel
    • Incidence of pseudoaneurysms requiring treatment: 3 - 6 %
    • Treatment: ultrasound-guided thrombin injection into the aneurysm, if necessary operative repair, esp. in aneurysms > 1,5 cm

    5. Endoprosthesis Migration

    • Displacement of the endoprosthesis by more than 5–10 mm from the original position, usually caudally
    • Incidence: 1 – 10 % (1-year follow-up after TEVAR)
    • Main cause of reinterventions in type I endoleaks (see below)

    7. Material Fatigue

    • Cause: fractures of stent struts, tears in endograft material, loosening of Prolene sutures that attach the endograft material to the stent struts
    • Consequence: Type I or Type III endoleaks (see below)

    8. Endograft Infection

    • Incidence after TEVAR: 0.4 – 3 %
    • Lethality 20 – 50 %!
    • Risk factors: age, diabetes, obesity, malnutrition, gangrene/ulcer, duration of preop. hospitalization, op duration, inguinal access, blood loss, reinterventions, lymphoceles, hematomas, seromas, wound healing disorders, wound infections
    • variable clinical presentation: relatively mild findings (elevation of inflammatory parameters), febrile infections up to dramatic courses with active bleeding/perforation, erosions of neighboring organs with fistula formations
    • Treatment: immediately after diagnosis broad-spectrum antibiotics; no pathogen detection in blood culture → vancomycin + agent against gram-negative pathogens (e.g. ceftriaxone, fluoroquinolone or piperacillin-tazobactam), otherwise according to resistogram; in case of infection persistence or recurrence after/or despite antibiotics → open surgical prosthesis explantation

    9. Endoleaks

    • Definition: persistent blood flow in the aneurysm sac after complete endograft placement
    • Classification using the example of abdominal aortic aneurysms:

    Type I

    lack of sealing of the landing zones

    • A: proximal anchoring
    • B: distal anchoring
    • C: iliac occluder in aortoiliac endograft and femorofemoral crossover bypass

    Type II

    retrograde blood flow in the aneurysm sac via collaterals (mostly inferior mesenteric artery and lumbar arteries, occasionally accessory renal artery)

    • A: single vessel
    • B: multiple vessels

    Type III

    • A: disconnection of prosthesis parts
    • B: defect in graft material

    Type IV

    porosity of the graft material (usually self-limiting)

    Type V

    endotension (aneurysm growth without endoleak detection)

    • Type I and Type III endoleaks are associated with a higher risk of aneurysm rupture → timely intervention recommended
    • Diagnostics: CT, MRI, contrast-enhanced color-coded duplex sonography
    • Treatment:

    Type I

    Intraoperative detection in the context of final sonography requires immediate correction, e.g.

    • targeted balloon dilatation or bare-metal stent implantation
    • extension of the endograft proximally or distally with an endograft cuff or additional stent grafts
    • attachment of the endograft material to the aortic wall using endostaples and endoanchors
    • transarterial liquid embolization using N-butyl cyanoacrylate or ethylene-vinyl alcohol copolymer

    Type II

    Indication for reintervention: endoleak detectable > 6 months and aneurysm size increase > 5 mm

    • transarterial liquid embolization
    • percutaneous, translumbar embolization (CT-/ultrasound-guided)
    • transvenous/transcaval embolization
    • clipping of a persistently open, large-caliber inferior mesenteric artery through MIC procedure using Endo-GIA

    Type III

    • placement of another endograft within the first endoprosthesis

    Type IV

    typical periprosthetic contrast cloud over several seconds at the time of the final control angiogram; usually stops within 24 hours as soon as heparin effect wears off and the pores of the graft material clog

    • no long-term side effects, requires no treatment  

    Type V

    possibly due to wave-like transmission of the pulsation of the stent graft wall through the thrombosed perigraft space to the native aneurysm wall

    Intervention only in case of aneurysm size increase with impending rupture (rare):

    • implantation of a second endoprosthesis within the first prosthesis
    • open surgical repair of the aneurysm with explantation of the endoprosthesis