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Complications - Chimney Technique for Juxtarenal Aortic Aneurysm (Ch-EVAR)

  1. Intraoperative Complications

    • Dissection and arterial thrombosis of the access routes, especially the brachial, axillary, and subclavian arteries as well as the lower extremities
    • Dissection, extravasation, and injury of the renal arteries during catheterization and placement of the covered stents
    • Dislocation of the covered stents.
    • Catheterization difficulties of the renal arteries
    • Perforation of the aortic sac with bleeding and shock state
    • Dissection and injury of the distal access routes (common femoral artery, pelvic arteries)

    → if interventional correction is not successful or critical bleeding occurs, immediate conversion to open surgery!

  2. Postoperative Complications

    1. Ischemic Complications

    Limb Ischemia  

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

    Pelvic Ischemia

    • due to embolization or coverage of the internal iliac artery with endoprosthesis → gluteal claudication, rectal ischemia, erectile dysfunction, skin or muscle necroses

    Prophylaxis:

    • Use of endoprostheses with iliac side branches to maintain pelvic perfusion

    Visceral Ischemia

    • due to coverage of the inferior mesenteric artery and/or thromboemboli
    • mostly colon affected, primarily descending colon and sigmoid
    • Clinical presentation: bloody stools, diarrhea, abdominal pain, peritonitis
    • Diagnostics: Rectosigmoidoscopy, possibly colonoscopy (Caution: increased risk of perforation!); Laboratory chemistry is nonspecific!
    • Therapy: conservative-wait-and-see only for transient mucosal ischemia/severity grade A, otherwise location-dependent bowel resection, possibly Hartmann procedure

    Severity Grades of Colonic Ischemia

    Damage

    Prognosis

    A

    transient ischemic colitis

    Restitutio ad integrum

    B

    Necroses of the tunica muscularis

    Defect healing, scar strictures

    C

    ischemic-necrotizing gangrenous colitis

    Colon gangrene

    Prophylaxis

    • preoperative exclusion of a significant stenosis of the superior mesenteric artery and the celiac trunk

    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

    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 probability 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 cerebrospinal fluid pressure

    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

    • Therapy:  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 perfusion (see above) are impaired and cannot be reopened by revascularizing measures
    • perioperatively sufficient central venous saturation (ScvO2) of ≥70 % and 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

    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 therapy
    • 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: temporary, 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
    • Therapy: symptomatic (antipyretic measures, antibiotics are not indicated)

    4. Pseudoaneurysms of the 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%
    • Therapy: ultrasound-guided thrombin injection into the aneurysm, possibly surgical repair, esp. for 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 EVAR)
    • Main cause of reinterventions for type I endoleaks (see below)

    6. Kinking/Occlusion of the Endograft Limbs

    • Incidence:  2 – 4 % of patients after EVAR
    • Causes: progressive shrinkage of the excluded aneurysm sac with consecutive deformation of the endograft, pronounced aortic neck angulation, narrower diameter of the distal aortic neck, which can lead to compression of the prosthesis limbs
    • Clinical presentation: intermittent claudication, also acute leg ischemia
    • Therapy: placement of bare-metal stents or additional stent grafts within the original endograft; for acute occlusion recanalization with thrombolysis and subsequent stent implantation

    7. Material Fatigue

    • Cause: fractures of the stent struts, tears in the 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 EVAR: 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), back pain, febrile infections up to dramatic courses with active bleeding/perforation, erosions of neighboring organs with fistula formations
    • Therapy: broad-spectrum antibiotics immediately after diagnosis; no pathogen detection in blood culture → Vancomycin + agent against gram-negative pathogens (e.g. ceftriaxone, fluoroquinolone or piperacillin-tazobactam), otherwise according to resistogram; for persistent or recurrent infection after/or despite antibiotics → open surgical prosthesis explantation

    9. Endoleaks

    • Definition: persistent blood flow in the aneurysm sac after complete endograft placement
    • most common complication after EVAR
    • Classification:

    Type I

    lack of sealing of the landing zones

    • A: proximal anchorage
    • B: distal anchorage
    • 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 the 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 → prompt intervention recommended
    • Diagnostics: CT, MRI, contrast-enhanced color-coded duplex sonography
    • Therapy:

    Type I

    Intraoperative detection during 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
    • ligation of a persistently open, large-caliber inferior mesenteric artery through MIC procedure using Endo-GIA

    Type III

    • placement of an additional 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 for 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