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Rutherford Vascular (derroberts)
Terms in this set (176)
What are the contraindications to endovascular treatment of AIOD?
There are no ABSOLUTE contraindications
1. Juxtarenal aortic occlusion
2. Juxtaposition to aneurysm disease
3. Hypoplastic aortic syndrome
4. Circumferential (>1 mm) calcification
What are some technical principles of axillofemoral bypass grafting?
Create axillary artery to graft anastomosis without tension when the arm is abducted by:
1. Placing the anastomosis as far medially as possible (this part moves far less than the more lateral part during abduction). This done by bringing graft into more nearly parallel relationship to the artery. Leaving the pectoralis minor muscle intact and tunnel the graft posterior to this muscle tends to force surgeon to keep the anastomosis medial
2. Allow some redundancy of the graft and even some bowing into the axilla posterior to the pectoralis minor muscle
Place the connection between the femorofemoral and axillofemoral components as close to the femoral artery anastomosis as possible so as to maximize flow throughout the entire length of the axillofemoral graft
What are the results of RCTs comparing CEA and BMT (NASCET, ECST, ACAS, ACST)?
What plaque and patient characteristics are associated with increased stroke risk in patients with carotid stenosis?
Which factors influence the decision to recommend intervention to patients with carotid stenosis in terms of patient-specific benefit (functional capacity, life expectancy)?
1. Life expectancy
- Symptomatic patients with high-grade stenosis can be considered for intervention when their life expectancy is 2-3 years
- However, asymptomatic patients should be expected to survive at least 3-5 years to derive significant benefit in stroke reduction with CEA
- Older age not associated with an increased risk of complications after CEA
- However, numerous studies indicate that older patients are at significantly higher risk of stroke (and to a lesser degree, death) after carotid artery stenting
- Most of the major RCTs have found a greater benefit from CEA in males versus females
- Severe studies suggest that CAS may be associated with more complications than CEA in women
4. Functional status
- The patient should have a baseline level of function sufficient that a further neurologic event would result in serious deterioration in functional or cognitive ability
- Patients with dense neurologic deficits unlikely to benefit; mild-to-moderate dementia or limitation in functional ability should be undertaken only after detailed and careful discussions
5. Cardiac status
- CEA associated with an increased risk of overall cardiac events compared with carotid stenting
- Predictors of adverse cardiac events include uncompensated CHF and untreated significant coronary disease
- Symptomatic 70-99%: clinical risk assessment alone; stress testing for those who are symptomatic with active angina, new onset EKG changes, or new onset CHF
- Full cardiac workup for asymptomatic
6. Renal insufficiency
- Excluded from major trials
Associated with features of plaque instability and increased complication rates after CEA and CAS
7. Contralateral carotid occlusion
- May be associated with a small-to-moderate increase in stroke after CEA but not CAS
Which factors are associated with a high risk for CEA and after CAS?
What recommendations regarding carotid intervention are shared by all major societies?
1. Symptomatic patients with stenosis <50% and asymptomatic patients with stenosis <60% - BMT
2. Control comorbid conditions, antiplatelet therapy, and statins and beta-blockers as indicated
3. CEA preferred over CAS in symptomatic patients with stenosis >50% unless contraindications to CEA (uncompensated cardiac disease or local scarring)
4. In symptomatic patients with stenosis >50% at high risk for CEA, CAS preferred over BMT
5. In patients with stroke or TIA, intervention should be performed within 2 weeks unless there are contraindications
6. In good-risk patients with asymptomatic stenosis >60%, CEA may be recommendation with BMT to reduce stroke risk if combined stroke and death rate <3%
7. In asymptomatic patients at high risk for intervention, neither CAS nor CEA has proven superior to BMT
8. Intervention not indicated for CTO of the ICA or with severe disability that precludes preservation of useful function
What are the societal guidelines regarding CEA and CAS in symptomatic and asymptomatic carotid stenosis patients?
Which patients are appropriate candidates for early 1-2 week CEA?
1. Mild to moderate deficits on the NIH stroke scale
2. No evidence of cerebral hemorrhage
3. <30% of the hemisphere involved in stroke
What are the outcomes of major trials comparing CEA and CAS for carotid artery stenosis?
What are guideline recommendations regarding use of CAS for SYMPTOMATIC carotid artery stenosis?
In SYMPTOMATIC patients deemed surgically unsuitable for CEA, CAS is recommended for use only in what situations?
By experienced operators
With a documented risk of death or stroke <6%
What are the guideline recommendations for treatment of ASYMPTOMATIC carotid artery stenosis?
What are CMS criteria for selection of patients to undergo CAS for carotid artery stenosis?
What are the 3 types of aortic arch and what are their definitions?
Type I aortic arches: great vessels arise at or above the same horizontal place as the OUTER CURVATURE of the arch
Type II aortic arches: origin of the innominate artery lies between the horizontal plane of the inner and outer curve of the aortic arch
Type III aortic arches: innominate artery lies below the horizontal plane of the inner curvature of the aortic arch
What are anatomic considerations regarding the choice to perform CAS in patients with carotid artery stenosis?
1. Aortic arch morphology
- Type III arches and a higher risk of embolic events
- Extensive aortic wall atheroma and irregularities (i.e., shaggy aorta)
- Severe calcification (eggshell aorta) - both increased complexity and increased risk of stroke
- Bovine aortic arch subtype II and I, "pure" bovine aortic arch
2. Carotid artery morphology
- ICA tortuosity, especially distally (difficulty in positioning EPD and more prone to vasospasm)
- Circumferential plaque burden and atheroma (increased risk of embolization and can make stent delivery difficult; inadequate stent expansion; and early restenosis due to recoiling)
3. Plaque morphology
- >10 mm in length (increased risk of stroke or death after CAS)
- Carotid plaque echolucency on Duplex increased risk of stroke
What is a "pure" bovine arch?
Common brachiocephalic trunk originates off aortic arch and then branches into:
- The right and left subclavian arteries
- A single bicarotid trunk
When should carotid artery stenting be performed?
- Data reporting outcomes after early CAS are inconsistent regarding whether outcomes may be worse when CAS is performed earlier
- Given that poor outcomes associated with early CAS were reported by early RCTs, use of early stenting in patients with recent cerebrovascular events should probably be approached with caution
In which patients is upper extremity access indicated for CAS for carotid artery stenosis?
1. Severe aortoiliac disease
2. Shaggy or eggshell aortas
3. Hostile neck
?Bovine aortic arch
?Type III arch
What types of embolic protection devices are available?
1. Filter-type EPDs
Advantages: 1) uninterrupted cerebral blood flow, 2) continuous access to angiography throughout the procedure, 3) low number of manipulations required within the carotid vessels
Disadvantage: 1) Filter must be passed through the carotid lesion prior to deployment
2. Distal occlusion balloon
Disadvantages: 1) requires passage of the carotid lesion prior to placement of embolic protection, 2) risk of incomplete evacuation of debris, 3) risk of distal ICA vasospasm or damage as a result of balloon deployment, 4) neurologic intolerance
3. Proximal protection EPDs
Advantages: 1) prevent the need for crossing the lesion prior to obtaining cerebral protection
Disadvantages: 1) large sheath required, 2) EPD manipulation in close proximity to the target lesion, 3) neurologic intolerance
When are nitinol carotid stents preferred?
- In general, nitinol carotid stents have a higher radial force than stainless steel stents
- They may therefore be more effective for highly calcified plaques with poor compliance
What are risk factors for persistent hypotension after carotid stenting (last 24-48 hours postoperatively)?
1. <=10 mm distance from the carotid bifurcation to the maximum stenotic lesion
2. Eccentric stenosis
3. Echogenic plaque morphology
4. Carotid bifurcation calcification
What are the recommendations for antiplatelet agents in patients with carotid artery stenosis undergoing CAS?
DAPT (ASA 31-325 mg plus clopidogrel 75 mg daily) starting 4 days before intervention and for 30 days after
What is the recommended postoperative surveillance after CAS?
Duplex US at 3-6 weeks, six months, and then annually
What are the recommended techniques to reduce periprocedural adverse events during CAS?
What is the epidemiology of carotid stenosis after radiotherapy?
Carotid stenosis after radiotherapy:
- Associated with an increased risk of cerebrovascular events
- Highest stroke risk after radiation for head and neck cancers
- Factors associated with the risk of developing carotid stenosis after neck radiation include older age, a history of smoking, heart disease, and treatment of malignancy without surgical resection
- Risk of developing carotid stenosis and associated cerebrovascular events increase with the passage of time after radiotherapy
Where does carotid artery stenosis after radiation present?
More diffuse and atypical locations than primary atherosclerotic disease:
- More likely to have disease in the CCA and distal ICA
- Radiation-induced lesion longer than the primary atherosclerotic lesion
- Maximal area of stenosis at the end of the stenotic lesion rather than the center, as seen in atherosclerotic disease
In patients with radiation-induced carotid artery stenosis, when should intervention be offered?
- Symptomatic patients: >50% stenosis BY ANGIOGRAPHY
- At least 80% in the asymptomatic patient and only if the periprocedural risk is low
What are the anatomic and physiologic factors affecting perioperative morbidity with carotid intervention (i.e., when is CAS, CEA, or BMT preferred)?
When might CEA be preferred over CAS in patients with radiation-induced carotid artery stenosis?
See Table 90. 1 (prior slide), but suggested in Rutherford's include:
1. Calcified type III arches
2. Near-occlusive or ulcerated plaque morphology
3. Young patients
What are the open reconstruction options for radiation-induced carotid artery stenosis?
1. Patch angioplasty (after endarterectomy)
2. Common carotid to internal carotid artery bypass with saphenous vein graft
3. Subclavian to carotid artery bypass
After CEA or CAS in the postradiotherapy patient, how should patients be treated or monitored?
- Antiplatelet medication indefinitely
- Physical examination and Duplex every 6 months for the first year and then annually thereafter
- Dual antiplatelets for 6 weeks
- Aspirin daily for life thereafter
- Physical examination and Duplex every 6 months for the first year and then annually thereafter
What is the epidemiology of recurrent carotid stenosis?
- Rate of restenosis over 2-5 years:
- Favors CEA
- For high-grade (>=70%) carotid resteonosis, 5-year risk of TIA/stroke is 23%, with most events happening in the first year
- Predictors of restenosis: age, female, history of head and neck cancer, diabetes, history of smoking, dyslipidemia, residual stenosis after stent placement, and large number of stents deployed
- Restenosis 5-times more common after CEA with primary closure vs when a patch is used
What is the postoperative Duplex examination after CEA?
- Duplex ultrasounds should be performed every 6 months for patients with stenosis >=50% on postoperative Duplex
- Intimal hyperplasia observed in early restenosis appears homogenous and echolucent on Duplex
- Late atherosclerotic recurrences demonstrate heterogeneity with marked luminal irregularity
What are the proposed Duplex criteria for in-stent carotid stenosis?
What are the indications to treat carotid restenosis?
1. Recurrent carotid stenosis >50% with symptoms (unless life expectancy is low or the patient has a high level of disability)
2. Asymptomatic stenosis >80% (decision should be individualized)
Although CAS is preferred over CEA for patients with recurrent carotid stenosis requiring treatment, when is CEA potentially not possible?
1. Type III arch anatomy
2. Extensive calcification
3. Ulcerated plaque morphology
4. Damaged stents
When might CEA be preferred to CAS in patients with recurrent carotid stenosis?
Young patients (given higher rate of restenosis after carotid stent placement)
What is the epidemiology of popliteal artery aneurysms?
- Found almost exclusively in men
- 50% have bilateral popliteal artery aneurysms
- 30-50% have an associated AAA
- <15% of patients with an AAA have a popliteal artery aneurysm
What are risk factors for development of ischemic complications among patients with asymptomatic popliteal artery aneurysms?
1. Aneurysm thrombus
2. Poor distal runoff
How are aortic tumors classified?
- Intraluminal or polypoid
- Intimal (polypoid and intimal) (most common)
- Mural (adventitial)
What is the etiology of stroke secondary to carotid artery stenosis?
3. Low flow state through the carotid artery
When are CTA and MRA indicated for workup of carotid artery stenosis?
1. Suspected disease proximal or distal to the neck
2. Indeterminate Duplex findings
3. Other confounding issues
How may use of selective shunting be determined intraoperatively during CEA?
1. Carotid "stump pressure" (<50 mmHg)
3. Somatosensory evoked potentials (SSEP)
4. MCA flow by TCD
5. Cerebral oximetry
6. Perform CEA under RA and insert shunt if symptoms develop after the carotid artery is clamped
What are the advantages and disadvantages of routine, nonroutine, and selective shunting during CEA?
- Allows CEA to be performed in a consistent manner
- Decreased surgeon and patient anxiety
- Placing a shunt relieves cerebral ischemia caused by clamping and decreases stroke rate and the inflammatory response of ischemic brain injury
- Stroke preventable with shunts
- Must use a test clamp (increased risk of embolization with unclamping and prolonged brain ischemia vs. routine shunting while shunt is placed)
- Stump pressure, TCD, or neurophysiologic monitoring not entirely reliable (only form of selective shunt that is truly reliable is neurologica examination during RA)
- Increases complexity of procedure
What are potential complications of saphenous vein patches for CEA?
1. Wound complications at harvest site
2. Compromise of a valuable conduit for later bypass procedures
3. Patch rupture (0.5-4% of cases) (GSVs with diameters <3.5 mm more prone to rupture) (using a GSV with a distended vein diameter >3.5 mm and maintaining a carotid bulb diameter >13 mm)
What are risk factors for recurrent carotid stenosis and indications for selective patching?
1. ICA diameter <6 mm
2. Female gender
3. Elevated cholesterol level
4. Possibly cigarette smoking and hypertension
What are the steps for managing a patient identified to have an intraoperative neurologic deficit after CEA?
1. Incision immediately reopened
2. ICA checked for flow with continuous wave Doppler
- If flow present, perform Duplex ultrasonography or angiography of the endarterectomy site and (if no cause found) intracranial imaging
3. If ICA has no flow, or if a local defect is suspected, re-explore endarterectomy site
- Meticulous search for a technical defect (e.g., distal intimal ledge)
- Best not to clamp distal ICA initially in the case of thrombosis and to extract the clob in the bulb and visible ICA so that backpressure may extrude any more distal ICA thrombus with the CCA clamped
- If no back flow, balloon catheter can be used
- If excessive platelet deposition occurred acutely at the endarterectomy site, resect the endarterectomy segment and replace with a 6 mm ringed PTFE interposition graft
What is the incidence of CN dysfunction after CEA?
What are the mechanisms of hypotension and hypertension after carotid endarterectomy?
- Endarterectomy of fixed atheromatous plaque at the bifurcation, with its chronic dampening effect on pulse pressure, creates a heightened sensitivity of the baroreceptor mechanism; persists until carotid sinus mechanism has been reset
- Closely correlated with preoperative hypertension
- Denervation of the carotid bulb
- Elevated cerebral norepinephrine or renin production
How is post-CEA hypotension and hypertension treated?
- Intravenous crystalloids
- Phenylephrine after to maintain systolic BP within 20 mmHg of the preoperative level
- IV sodium nitroprusside
- Maintain systolic BP within 20 mmHg of the preoperative level
What are the risk factors for development of recurrent carotid stenosis?
6. Primary closure
In which patients would you perform a staged or combined CEA and CABG?
Staged (CEA then CABG in 1-2 days):
- Symptomatic significant ICA stenoses
- Bilateral severe asymptomatic stenoses
- Significant carotid artery disease and severe 3-vessel or left main coronary disease and/or critical aortic stenosis
What are the NICE recommendations regarding claudication?
The Global Vascular Guidelines (GVG) recommends that decisions regarding revascularization are based on PLAN principles. Define PLAN principles.
Patient risk estimation:
- Candidacy for limb salvage
- Peri-procedural risk
- Life expectancy
Limb threat severity (SVS Wound Ischemia foot Infection staging system)
ANatomic pattern of disease using the GLobal Anatomic Staging System (GLASS) based upon high-quality imaging that should include the foot and ankle, together with an assessment of the availability and quality of autogenous vein for bypass
What is the basis for the GLASS framework and how is it used?
Bypass surgery requires adequate inflow and a suitable autogenous conduit
Success of endovascular treatment largely defined by the burden and complexity of atherosclerosis within the anticipated target artery path (TAP)
Defining the planned endovascular treatment TAP in each individual case is the basis for the GLASS framework
- In defining the overall GLASS stage (I-III) for the limb, GLASS combines grade scores (0-4) from both the femoropopliteal segment (origin of the SFA to the origin of the AT artery) and the infrapopliteal segment (origin of the TPT and the AT to the malleoli)
- There are modifiers for heavy calcification and inframalleolar disease
The intention is that GLASS stage will be used to help predict the likelihood of technical failure and 12-month limb-based patency (LBP) (in-flow flow) as follows:
- Stage I: Average complexity: expected technical failure <10% AND >70% 12-month LBP
- Stage II: Intermediate complexity: expected technical failure <20% AND 50-70% 12-month LBP
- Stage III: High complexity: expected technical failure >20% AND <50% 12-month LBP
What are the GLASS grades for the femoropopliteal and infrapopliteal segments?
What are the GLASS grades for the femoropopliteal and infrapopliteal segments?
What are favorable and unfavorable characteristics of arch vessel disease?
What are the theories of the etiology of inflammatory aneurysms?
Theories of the etiology of inflammatory aneurysms:
1. Exaggerated variation of the normal inflammatory response
2. Chronic subacute rupture
3. Variant form of retroperitoneal fibrosis
What is Cogan's syndrome?
- May present with large and medium-sized vasculitis in a Takayasu's-like distribution
- Immune-mediated disorder characterized by interstitial keratitis, vestibular dysfunction, and sensorineural hearing loss
- Keratitis symptoms include bilateral redness, pain, photophobia, and lacrimation
- Uveitis, scleritis, choroiditis, and retinal artery occlusion may occur with or without keratitis
- Vestibular dysfunction presents with tinnitus, vertigo, and sensorineural hearing loss
- Mean age of onset 30 years and equally distributed in men and women
What inflammatory conditions are associated with an increased risk of aneurysmal degeneration?
1. Takayasu's arteritis
2. Giant cell arteritis
3. Polyarteritis nodosa
4. Behcet's disease
5. Cogan's syndrome
6. Cystic medial necrosis
What is the risk of having a AAA in patients with a family history of aneurysmal/AAA disease?
Patients with a family history of aneurysm disease have a 30% increased risk of having an aneurysm
What are the risk factors for AAA development?
1. Older age
2. Smoking and duration of smoking
3. Family history of aortic aneurysm
5. History of MI
6. Peripheral artery disease
Negative risk factors include:
1. Female gender
3. African American race
What are risk factors for popliteal artery aneurysms?
Similar to AAAs:
1. Older age
2. Male gender
3. Presence of other arterial aneurysms
5. Family history
6. Cardiac disease
8. Atherosclerotic disease
Risk factors for popliteal artery aneurysms are missing PAD, but include male gender and presence of other arterial aneurysms (vs. AAA risk factors)
What are the risk factors for AAA rupture?
1. Female gender
2. Larger initial AAA diameter
4. Lower FEV1
5. Higher mean BP
This was as reported by the UK Small Aneurysm Trial
What is the 12-month risk of rupture based on AAA diameter?
What features aside from AAA diameter correlate with increased risk of AAA rupture?
1. Saccular morphology
2. Certain CTA characteristics:
- Presence of a dissection
- Mural thrombus
- Dissection of the peripheral calcification of the aneurysm sac
The presence of intraluminal thrombus has been associated with what events in patients with AAAs?
1. Wall thinning
2. Medial loss of smooth muscle cells
3. Elastin degradation
4. Adventitial inflammation
5. Aortic wall hypoxia
What are connective tissue syndromes associated with abdominal aortic aneurysms?
What are the indications for open vs. endovascular AAA repair?
- No or hostile aortic neck
- Narrowed or calcified aortic bifurcation
- Iliac artery occlusive disease
- Concomitant common or external iliac artery aneurysms, especially when internal iliac artery patency needs to be preserved (claudicants, patients at risk for colonic, pelvic, and spinal cord ischemia)
- Horseshoe kidney with multiple renal and isthmus arteries originating from the aorta and iliac arteries
- IMA patency needs to be preserved (bilateral internal iliac artery occlusion, SMA stenosis/occlusion, previous colectomy)
- Migration or recalcitrant endoleak not able to be resolved by endovascular means
What are the advantages and disadvantages of the transperitoneal approach to AAAs?
1. Rapid access (ideal for emergencies)
2. More familiar and comfortable approach for many surgeons
3. Better access to right renal artery and right internal and external iliac arteries
4. Ability to examine bowel after repair and perform complete abdominal exploration
1. Hostile abdomen: multiple previous abdominal operations, stoma, radiation
2. Inflammatory aneurysms
3. Horseshoe kidney with multiple renal and isthmus arteries
4. More difficult to expose visceral aortic segment
What are the advantages and disadvantages of a retroperitoneal approach to AAAs?
1. Superior exposure of the visceral and supraceliac aortic segment
2. Better exposure of the left renal artery
3. Inflammatory aneurysms
4. Horseshoe kidney
5. Avoid adhesions and hostile abdomen from previous abdominal operations/stoma
6. Ideal for obese patients (abdominal contents fall away)
7. Decreased postoperative fluid requirements
8. Decreased pulmonary edema
9. Decreased respiratory failure
10. Lower rates of ileus and SBO
11. Shorter length of ICU and overall hospital stay
12. Shorter time to full recovery
1. Limited familiarity to many surgeons
2. Limited visualization of abdominal contents
3. Difficult or limited exposure of right femoral, iliac, and renal arteries
4. Increased incisional pain and long-term wound problems
What are the indications to preserve the IMA during open AAA repair?
1. Significant SMA disease
2. Bilateral hypogastric artery occlusions
3. Prior colectomy
4. Large IMA
5. Sluggish or no backbleeding from an IMA that is known to be patent
6. Evidence of colonic ischemia upon completion of aortic repair
What are the risk factors for colon ischemia after AAA repair?
1. Ligation of the IMA
2. Failure to revascularize the hypogastric arteries
3. Iliofemoral occlusive disease
4. SMA stenosis
5. Prior colectomy
7. Retractor injury
What are the risk factors for spinal cord injury during AAA repair?
Risk factors for spinal cord injury during AAA repair:
1. Extent of proximal coverage
2. Previous thoracic aortic procedures
3. Aortic cross-clamp location
4. Aortic cross-clamp duration
5. Patency of internal iliac arteries
6. Profound intraoperative or postoperative hypotension
What are the risk factors for EVAR migration?
1. Angulation of the neck
2. Decreased neck length
3. Neck thrombus
4. Large diameter of the neck
What are the risk factors for EVAR graft limb occlusion?
1. Aortoiliac occlusive disease
2. Small distal aorta (<14 mm)
3. Tortuous iliac arteries
4. External iliac artery landing
What are the predictors of AAA neck dilation?
1. Large AAA diameter
2. Large aortic neck size
3. Circumferential neck thrombus
What are the risk factors for peripheral artery disease?
What are key components of a structured exercise program for claudication?
What is the pharmacologic treatment of claudication?
What are the definitions of MACE, MALE, and other outcomes defined by the SVS Working Group?
See Table 105.2
What are relative indications for aorto-uni-iliac endograft devices?
What are contraindications to percutaneous access for EVAR?
What are risk factors for colon ischemia after ruptured AAA repairs?
1. Degree and duration of hypotension
2. Patency of the IMA
3. Collateral supply between the SMA, IMA, and internal iliac arteries
What are risk factors for abdominal compartment syndrome after ruptured AAA?
1. Use of an aortic occlusion balloon
2. Massive blood transfusions
4. Hemodynamic instability
What are risk factors for spinal ischemia after ruptured AAA repair?
1. Interruption of pelvic blood supply
2. Prolonged aortic cross-clamping
3. Preoperative and intraoperative hypotension
What are risk factors for respiratory failure after ruptured AAA repair?
1. Administration of large volumes of fluid and blood products
2. Long cross-clamp times
What are risk factors for renal dysfunction after ruptured AAA repair?
1. Suprarenal cross-clamping
2. Longer duration of cross-clamping
3. Preexisting renal insufficiency
5. Increased age
What are etiologies for iliac artery aneurysms?
3. Previous trauma
4. Iatrogenic injury
6. Connective tissue disorders
7. Infections (Salmonella, Staphylococcus, Klebsiella, Candida, Syphilis, TB)
What are the presenting signs and symptoms of an iliac artery aneurysm?
1. Vague lower abdominal pain
2. Intermittent claudication or lower extremity pain (embolic arterial occlusion)
3. Lower extremity paresis, sciatic neuralgia, or lumbosacral pain
4. Ureteral obstruction
7. Sudden abdominal, groin, or flank pain with hemorrhagic shock (rupture)
What is the indication for repair of internal iliac artery aneurysms (isolated)?
1. >=3.5 cm in healthy patients
2. Symptomatic (rupture, compression of surrounding structures--ureter, colon/rectum, sciatic nerve or lumbosacral plexus, iliac veins, etc.)
What is the classification scheme for endovascular treatment of isolated iliac artery aneurysms?
What is important when performing internal iliac artery embolization?
1. Embolize the proximal main trunk of the artery to avoid occlusion/maintain patency of distal hypogastric branches
2. Maximize ipsilateral external iliac and common femoral arterial flow to provide collaterals to compensate for ipsilateral internal iliac artery occlusion
3. Stage internal iliac artery embolizations if bilateral
4. Stage unilateral embolizations (see my previous notes)
What are the staging criteria for severity of clinical symptoms after intentional internal iliac artery occlusion?
Class 0: no symptoms
Class I: nonlimiting claudication with exercise
Class II: new onset impotence, with or without moderate to severe buttock pain, leading to physical limitation with exercise
Class III: buttock rest pain, colonic ischemia, or both
What are risk factors for pelvic ischemia after unilateral iliac artery occlusion/embolization on preoperative angiography?
1. Stenosis of the remaining internal iliac artery >70% with nonopacification of 3 of the 6 typical internal iliac artery branches
2. Small-caliber, diseased, or absent ipsilateral medial and lateral femoral circumflex arteries
What are the epidemiologic or clinical presentation differences between aortic dissection and PAU?
1. PAUs are most frequently found in elderly male patients in their 7th to 8th decade of life (patients with PAUs are considerably older than those with other aortic pathologies, except aneurysms, and are generally a decade older than patients with AD)
2. As with IMH and AD, patients with PAUs almost universally have a concurrent history of hypertension (92%)
3. Unlike IMH and AD, patients with PAU are generally infirm with multiple serious comorbidities, including smoking, CAD, COPD, and PAD
4. Rupture associated with PAU is more common than rupture associated with AD (in symptomatic patients with PAU, 9-44% were found to have aortic rupture)
5. Physical exam findings may distinguish patients with PAU vs. AD:
- Patients with PAU seldom have aortic valve regurgitation (frequently observed with type A AD)
- Peripheral pulses typically equivalent in upper and lower extremities with PAU (may not be equivalent with AD)
- Patients with AD may present with neurologic deficits, mesenteric malperfusion, and renal failure, which are not typically found in patients even with symptomatic PAU
6. Patients with PAUs often have large aortic diameters at diagnosis, and multiple groups have noted an association between PAU and AAA. The incidence of AAA associated with PAU is higher as compared with type A and B dissections
How do patients with PAU present clinically?
- Chest pain
- Shortness of breath
- Neck and jaw pain if ascending aorta involved
- Tearing or ripping back pain (similar to AD)
- Upper back, mid-scapular, and abdominal pain if arch and descending aorta are involved
- Asymptomatic (only 9%; generally, >75% present with acutely worsening pain for <2 weeks; abdominal PAU not infrequently present asymptomatic)
- Rupture (9-44% of symptomatic present with rupture)
- Pulmonary complications (pleural effusions or an enlarging hemothorax--suggest acute presentation and impending rupture irregardless of pain)
- Atheroembolism (abdominal instead of thoracic PAUs are more likely to cause embolization and distal ischemia)
How are PAUs assessed on CT for ulcer dimensions?
1. Maximum width of the entry defect from the lumen
2. Maximum depth from the lumen to the aortic wall
3. Maximum length of the intramural component of the ulcer itself
What are recommended treatments for conservative management of asymptomatic PAUs?
- conservative treatment preferred in patients presenting with an isolated PAU without associated symptoms or if symptoms well controlled with antihypertensive medications
1. Strict BP control with beta-blockade or vasodilators
2. Treatment of hyperlipidemia
What are the indications for treatment of PAUs?
1. Failure of medical management to control pain or BP
2. Signs of impending or contained rupture (rapidly growing ulcers, periaortic hematoma, hemothorax, and pleural effusions)
3. Aortic diameters >60 mm adjacent to a PAU, PAU diameter >20 mm, and PAU depth >20 mm
4. Signs of progression or impending vascular compromise (expanding IMH, evolving AD, distal embolization, hemodynamic instability)
What are sizing and balloon-related suggestions for TEVAR of PAUs?
1. Only a 5 to 10% maximum oversizing should be performed
2. Balloon dilation should only be done in areas of stent graft overlap, and not in the landing zones or around the region of the PAU
3. CSF drainage not uniformly recommended given focal nature of PAUs
What are risk factors for mortality after TEVAR for PAUs?
1. Emergent vs. elective repair
2. History of CHF
3. Perioperative stroke
4. Need for dialysis
What are risk factors for treatment failure with TEVAR for PAUs?
1. Increased aortic diameter adjacent to PAU
2. Other aortic pathology (IMH)
What are the causes of hand/upper extremity ischemia?
Which arterial diseases affect which upper extremity arteries?
What is the pathophysiology of DFUs?
What are the Wagner and Texas Classification Systems for DFUs?
How are noninvasive vascular studies interpreted in the diabetic foot?
What are the complications of aortobifemoral bypass?
What are the primary indications for axillofemoral bypass?
1. Symptomatic aorta and/or biiliac arterial occlusive disease at excessively high risk for direct aortic repair
2. Infected native aortas or aortic grafts or aortoenteric fistulas
3. Hostile abdomen (multiple previous surgeries, active intra-abdominal infection, intestinal or urinary stomas)
When is a retroperitoneal approach indicated for conduct of an ABF for AIOD?
1. Multiple prior abdominal operations
2. Abdominal wall stoma
3. Concurrent renal or mesenteric arterial disease requiring suprarenal exposure
4. Severe cardiopulmonary disease
Clear disadvantages include accessing the right renal and iliac arteries and the right groin, particularly in obese patients
When is a renal artery revascularization indicated in patients undergoing surgery for AIOD?
1. Multidrug-refractory hypertension
2. Ischemic nephropathy with reversible component
3. Accessory renal arteries arising from the diseased aortic segment
When is a combined inflow and outflow procedure indicated in patients with AIOD?
- Atretric or prohibitively diseased profunda and a severely diseased SFA
In deciding whether to perform a staged or simultanous repair, must weight:
- Ability of patient to tolerate a prolonged operative procedure
- Risk of wound and graft infection from repeat groin dissection
- Risk of progressive tissue loss during the initial recuperation period
In which circumstances may aortobiiliac bypass (external iliac arteries) be preferable to aortobifemoral bypass?
1. Hostile groin creases from prior surgery or radiation therapy
2. Obese patients
3. Diabetic patients with an intertriginous rash at the inguinal crease
- AND PATENT EXTERNAL ILIAC ARTERIES
What vascular lab workup predicts outcomes in diabetic patients?
NB: TBI >0.7 is considered normal in all patients
Healing unlikely to occur if:
- PVR amplitude <5 mm
- Photopletysmography (PPG) <50 mmHg
- tcPO2 index <0.4 (tcPO2 index determined by dividing foot tcPO2 by a reference point tcPO2 at the chest)
- Skin perfusion pressure <30 mmHg
Wound healing likely to occur if:
- TBI >0.6
- tcPO2 > 40 mmHg
- tcPO2 index >0.6
- Skin perfusion pressure >60 mmHg
What are the muscle and bony abnormalities that can occur in the diabetic foot?
1. Hallux valgus
2. Hallux limitus
3. Hallux malleus (ie, hammertoe)
4. Clawed toes
5. Adductovarus toe
7. Prominent sesamoids
8. Elongated or declined metatarsal heads
9. Charcot foot
What are the essentials of the diabetic foot exam?
What is the classification system of diabetic foot infection by the International Working Group on Diabetic Foot Infection
Note similiary to fI of SVS WIFi
PEDIS (perfusion, extent, depth, infection, and sensation)
What are the risk factors for DFU formation?
1. Peripheral neuropathy
3. Soft tissue infection
4. Biomechanical abnormalities
5. Peripheral edema
6. Plantar callus formation
8. Poor glucose control
10. Prolonged diabetic course
What tests should be done to diagnose upper extremity arterial disease?
Also segmental arterial pressures in the upper extremities and Duplex of the axillosubclavian segment
What should be looked for on physical examination in patients with suspected upper extremity ischemia?
1. Brachial and forearm BPs, at rest and 2-5 minutes after exercise (gradient of 20 mmHg between arms considered significant)
2. All pulses palpated; Doppler insonation of the radial, ulnar, palmar, and digital arteries
3. Auscultation of the supra- and infraclavicular fossae
4. Hands and digits examined for temperature, capillary refill, and ulcers
5. Fingers examined for clubbing, sclerodactyly, telangiectasia, and nail bed splinter hemorrhages
6. Upper extremity neurologic examination
What is the TASC classification for AIOD?
What are the recommendations regarding preventive measures for intra-arterial and intravenous contrast and CIN?
- eGFR <60 mL/min and intra-arterial contrast: full preventive measures
- eGFR <45 mL/min and IV contrast: full preventive measures
What precautions should be performed to reduce risk of CIN?
1. IV hydration--either NS or sodium bicarbonate; if sodium bicarbonate is used, the initial IV bolus is 3 mL/kg/h (154 mEq/L sodium bicarbonate in dextrose and water) for 1 h immediately prior to contrast injection followed by administration at a rate of 1 mL/kg/h for 6 h
2. Use lowest volume of contrast (<5 mL/kg)
3. Avoid repeat contrast injections within 72 h
4. Diruetics witheld on day of contrast injection
5. Metformin held as per other guidelines (48 h before if CKD or on the day of if normal renal function)
What are risk factors for failure of endovascular management of AIOD?
1. Female gender
2. Small vessel diameter
3. Renal insufficiency
5. Extension of disease into the EIA
What are the criteria for an iliac stent restenosis?
1. >50% diameter reduction
2. Doubling of PSV
3. Drop in ABI >0.1
What is the TASC score for AIOD and FP disease?
In which patients should infrainguinal bypass be delayed to allow cardiac evaluation?
1. Unstable angina
2. Recent MI
3. Poorly controlled CHF
4. Critical aortic stenosis
5. Symptomatic/untreated arrhythmia
Invasive coronary intervention should only pursued only if: 1) patient and anatomic characteristics are favorable, 2) benefit-to-risk ratio is high, and 3) delay to perform the intervention is not prolonged
What are the prediction scores and their elements for outcome after infrainguinal bypass?
What are the indications (evidence-based, relative expanded) and contraindications to vena cava filter placement?
See Box 152.1
What are risk factors for thoracic and thoracoabdominal aortic aneurysms?
4. Chronic dissection
5. Connective tissue diseases (Marfan's disease, thoracic aortic aneurysm and dissection or TAAD)
What are risk factors for thoracoabdominal aortic aneurysm rupture?
What is the etiology of thoracoabdominal aortic aneurysms and the relative percentage contributing to disease?
What is the Crawford classification of thoracoabdominal aortic aneurysms?
What are recommendations for physical examination of the patient presenting with thoracic aortic aneurysm?
What are recommendations for thoracic and thoracoabdominal aortic aneurysm repair?
What are recommendations for preoperative evaluation of patients undergoing thoracoabdominal aortic aneurysm repair?
What are risk factors predictive of perioperative mortality following thoracic endovascular aneurysm repair?
What are 6 adjuncts during open thoracoabdominal aortic aneurysm repair that can be used to maximize spinal cord perfusion?
2. Spinal fluid drainage
3. High MAP
4. Maintenance of tissue oxygen delivery (avoid anemia, hypoxia; maintain cardiac index)
5. Neurochemical protection (naloxone, steroids, barbiturates); avoid vasodilators (nitroprusside, hydralazine)
6. Intercostal reimplantation
What factors are associated with increased paralysis as per the Expected Paralysis Model in patients undergoing TAAA repair?
1. Poor cardiac index
3. Crowford type II
4. Acute dissection
5. No spinal fluid drainage
What measures should be taken in the event of delayed paraplegia after TAAA repair?
1. Increasing MAP
2. Increasing cardiac index
3. Draining spinal fluid - aim for spinal fluid pressure <6 mmHg
4. Restarting neuroprotective medications
What are the indications for repair of thoracic aortic aneurysms with TEVAR or open repair?
1. Diameter >=5.5-6 cm with saccular morphology
2. Rapidly expanding aneurysms
3. Symptomatic aneurysms
In which situations is the durability of TEVAR questionable/relative contraindications when repairing thoracic aortic aneurysms?
1. Large diameter necks
2. Angulated aortic segments
3. Circumferential thrombus lining the seal zones
4. Significant angulation of the arch (>60-degrees) adjacent to the proximal portion of the aneurysm
5. Life-threatening allergies to IV contrast or to nickel or stainless steel
6. Those who cannot be monitored reliably
What are the options for debranching of zone 1 or zone 0 during TEVAR?
1. Right CCA-to-left CCA bypass (6-8 mm PTFE retroesopagheal)
2. (Right carotid inflow inadequate): Left common femoral artery to left axillary artery then from left subclavian artery to left CCA
3. Endovascular: Exposure of left CCA and retrograde CCA covered stent deployment (Chimney technique) during transfemeoral TEVAR deployment
1. Open arch debranching via median sternotomy and bifurcated prosthetic graft sewn to the ascending aorta, innominate artery, and left CCA
See Figure 78.9 for zone 0/1 options (important Figure, with options including left CCA to left SCA with or without left CCA after bifurcated graft to innominate and left CCA; right CCA to left SCA with implantation of the left CCA onto the bypass graft; snorkeling of the innominate or left CCA with bypasses)
What are the options for debranching in aortic zones 0 and 1?
See Figure 78.9
How may the distal seal zone in TEVAR be extended if there are insufficient collaterals between the SMA and celiac arteries or if both SMA and celiac arteries must both be covered
One option is the use of periscope grafts (self-expanding covered stents inserted into the celiac artery +/- SMA via femoral or other access)
How should TEVARs be surveilled?
CT at 1 month and 1 year
What is a risk factor for stroke with TEVAR?
1. Deployment of the endograft proximal to the left CCA
2. Female sex
3. Prolonged procedure time (>160 minutes)
What are risk factors for spinal cord ischemia after TEVAR?
1. Concomitant or previous infrarenal aortic repair
2. Extensive thoracic aortic coverage
3. Renal insufficiency
4. Intraoperative hypotension (systolic BP <80 mmHg)
5. Coverage of the hypogastric artery
6. Coverage of the left subclavian artery
What are methods to reduce spinal cord ischemia after TEVAR?
1. Intraoperative hypothermia (34 C)
2. Intraoperative naloxone, mannitol, and steroids
3. Avoidance of arterial vasodilators
4. MAP 90-100 mmHg
5. Hemoglobin >=100 g/dL
6. Spinal drain
What are complications of TEVAR for thoracic aortic aneurysms?
1. Vascular complications (iliac artery injuries, vascular access complications)
2. Neurologic complications (stroke and SCI)
4. Sac enlargement
When is a hybrid approach (debranching and TEVAR/EVAR) considered for patients who meet standard criteria for repair of their aneurysms, and when is it relatively contraindicated?
1. Patient with significant pulmonary compromise but adequate cardiac and renal function (e.g., advanced COPD)
1. Poor cardiac function
2. ESRD requiring hemodialysis
3. Lack of healthy distal aorta or iliac artery
4. Insufficient landing zones
What are the main society guidelines on management of thoracic aneurysmal disease?
During TEVAR, what are the requirements for the proximal aortic neck or sealing zone?
1. Length of the sealing zones >=2 cm and ideally larger
2. Without thrombus or dissection, and with a consistent diameter (parallel walled aorta)
3. Maximum aortic diameter 38 mm, with clearly hostile neck >42 mm
4. Minimum overlap of 30 mm when multiple stent grafts used
5. Oversizing of 10-20% at the proximal landing zone (some authors 10-15% for degenerative aneurysms)
6. For a previous Dacron graft, longer length (4-5 cm) of overlap and more aggressive oversizing recommended
What are techniques to deal with poor iliac access during TEVAR?
1. Balloon angioplasty of limited stenoses of the iliac arteries
2. Retroperitoneal access: marginal common femoral arteries, highly tortuous external iliac arteries (pull on the artery to straighten the vessel)
3. Direct puncture of the common iliac artery or anastomosis of an iliac conduit to the CIA
4. Paving and cracking technique (deploying a 10-mm or 13-mm self-expandable covered stent in the CIA or EIA and then cracking with a 10- or 12-mm balloon)
Which factors are predictive of both rupture and deployment failure during TEVAR?
1. Severe iliac and aortic calcification, angulation, and tortuosity
2. Iliac diameter <8 mm
What are rescue techniques if a TEVAR device migrates proximally and covers a supraaortic trunk vessel?
1. Manual balloon traction
2. Parallel stent placement (chimney or stenting of the target vessel)
3. Open conversion
What are the neuroprotective strategies during TEVAR?
1. Intrathecal papaverine
2. Naloxone, mannitol, and steroids
3. Ischemic preconditioning by staged repair
4. Intraoperative hypothermia (34 C)
5. Deliberate hypertension (MAP=90-100 mmHg)
6. Avoiding vasodilators
7. CSF drainage with lumnbar drain maintained at 10 cmH2O for 48 h
8. Preserve the collateral network supplying the spinal cord (left subclavian, intercostal, lumbar, and internal iliac arteries)
9. Maximize oxygen delivery (Hgb target >100 g/L and SpO2 >95%)
What are the risks of CSF drainage?
1. Catheter fracture
2. Postdural puncture headache
3. Neuraxial hematoma
4. Intracranial hemorrhage (subdural, cerebellar, subarachnoid, intraventricular, and intraparenchymal hematomas)
What are the risk factors for stroke during TEVAR?
2. Chronic renal failure
3. Known cerebrovascular disease
4. Increased aortic coverage
5. Female gender
6. Longer surgery duration
7. Occlusion of the left subclavian artery
What are risk factors for retrograde type A dissection during TEVAR (which occurs in 2% of case, >2/3 occurs in the perioperative period, and 25% asymptomatic presentations, and mainly occurs after treatment of type B dissection and especially acute presentations, but also thoracic aneurysm repair)
3. More proximal landing zone
4. Manipulation of guidewires and sheaths
5. Progression of the underlying diesease
What is the definition of stent graft migration?
Caudal or cranial movement of the stent graft with respect to the native vasculature >10 mm or any distance that results in clinical sequelae or a secondary intervention
What are the CTA signs of TEVAR stent graft infection?
1. Aortic wall thickening
2. Perigraft soft tissue >5 mm between an adjacent organ and the stent graft
3. Fluid collection
4. Perigraft air (>6 weeks after surgery) or increasing air on serial imaging examinations
5. Adjacent soft tissue stranding
6. Abscess formation
7. Graft thrombosis or expansion
What is the treatment for TEVAR stent graft infection?
Complete removal of the infected stent graft and wrapping of the replacement graft with pedicled omentum, in association with optimum antibiotic treatment (cryoallograft, neoaortoiliac system, or an antibiotic-soaked prosthetic)
What factors are associated with operative mortality after TEVAR?
1. Age >=70
2. BMI <30 kg/m2
3. COPD requiring total functional assistance
4. BUN >25 mg/dL
5. WBC count >12
6. Emergency operation
7. Left subclavian artery coverage
8. Thoracoabdominal extension
9. Mesenteric debranching
What are the DeBakey and Stanford classifications of acute aortic dissection?
Where is the origin of the entry tear in patients with acute aortic dissection?
1. Ascending aorta (65%) (most commonly at the sinuses of Valsalva or sinotubular junction in patients <40 years or higher in the ascending aorta in older patients)
2. Descending aorta (25%) (most often within a few cm of the LSCA)
3. Arch and abdominal aorta (10%)
What is the usual pattern of Stanford type B dissection?
Cleavage plane progresses with the distal false lumen on the left posterolateral aspect of the aorta (80%); the celiac, SMA, and right renal arteries typically emanate from the true lumen, and the left renal artery arises from the false lumen
What are the two mechanisms for aortic branch compromise after aortic dissection?
1. Dynamic obstruction:
- The compressed true lumen is unable to provide adequate volume flow, or the dissection flap may prolapse into the vessel ostium, which remains anatomically intact
- The septum may prolapse into the vessel ostium during the cardiac cycle, and the compressed true lumen flow is inadequate to perfuse branch vessel ostia which remain anatomically intact
- Responsible (at least in part) for >80% of malperfusion syndromes
- The severity of the true lumen collapse and the degree of aortic-level ostial vessel occlusion is determined by: 1) the circumference of the dissected aorta, 2) cardiac output, 3) BP, 4) HR, and 5) the peripheral resistance of the outflow vessel
2. Static obstruction:
- Malperfusion is caused by the dissecting process extending into the branch vessel proper, narrowing it to a variable degree
- False lumen is highly thrombogenic as a result of the exposed adventitial and medial layers, and thrombus formation may form in the blind end of the dissection
- This obstruction is unlikely to resolve with restoration of aortic true lumen flow alone, and some manipulation of the vessel itself (e.g., stent or bypass graft) will typically be required
What is the clinical presentation of patients with acute aortic dissection?
1. Pain (back, abdomen, or chest; typically anterior with type A and in the back with type B)
3. Syncope/neurologic symptoms (stroke, spinal cord ischemia, direct compression of peripheral nerves with paresthesias from lumbar plexopathy, hoarseness from RLN involvement, or Horner syndrome from compression of the sympathetic ganglion)
4. Peripheral vascular complications (brachiocephalic trunk, CCAs, LSCA, and ilieofemoral arteries)
What is the only indication for ACUTE OPEN graft replacement in patients with type B dissection?
Threatened or actual rupture at the aortic intimal tear in the proximal descending aorta with no identifiable proximal seal zone
When indicated, what are the goals of TEVAR for acute type B dissection?
1. Coverage of the proximal entry tear
2. Expansion of the true lumen with restoration of flow to visceral vessels
3. Obliteration of false lumen flow with subsequent complete thrombosis
What is the open surgical treatment of malperfusion syndrome after type B dissection?
See Figure 81.8 for details
What are the risk factors for aneurysm development after type B dissection (and predictors of patients who will benefit from elective coverage of the entry tear with a TEVAR)?
1. Poorly controlled hypertension
2. Maximal aortic diameter >=4 cm in the acute phase
3. Continued patency of the false lumen
4. Proximal entry tear >=10 mm
5. Partially thrombosed distal false lumen
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