Endovascular Repair of Abdominal Aortic Aneurysms

Question 1

Crawford Classification of Thoracoabdominal Aortic Aneurysms

Answer 1

Crawford Type I Thoracoabdominal Aneurysm: originates below left subclavian artery (third/last great vessel off aorta) and extends to involve the celiac axis and mesenteric arteries, but doesn’t reach to or past the renal arteries
Crawford Type II Thoracoabdominal Aneurysm: originates below the left subclavian artery (third/last great vessel off aorta) and extends into the infrarenal abdominal aorta
Crawford Type III Thoracoabdominal Aneurysm: originate in lower descending thoracic aorta (so well beyond left subclavian artery, specifically originating in the lower thoracic aorta below the 6th rib) and involve the entire remainder of the aorta
Crawford Type IV Thoracoabdominal Aneurysm: originate at the diaphragm (so even lower origination than type III) and involvethe abdominal aorta only
Crawford Type V Thoracoabdominal Aneurysm: originate below the 6th rib (the lower thoracic aorta, like type III) and extend only to the renal arteries

Type II and III = most complicated to repair. Can remember because they extend down the furthest, so they include the most major branches off the aorta
Type II repair = greatest risk for paraplegia and renal failure, which makes sense because this just involves the very most thoracoabdominal aorta

Notice that all of these classifications are for descending thoracic and abdominal aortic aneurysm - NONE start proximal to the left subclavian artery.

Question 2

Aneurysm vs Pseudoaneurysm vs Dissection

Answer 2

Aneurysm = dilation of all 3 walls of the artery (Intima, Media, and Adventitia) but they are all intact

Pseudoaneurysm = tear through all 3 layers of the vascular wall results in formation of an extravascular hematoma (outside the arterial wall), yet contained by surrounding tissue, and remains in free communication with the intravascular space.

Dissection = tear through usually just the intima, but maybe the Media too, so that blood forms a channel in the wall of the blood vessel itself

Question 3

Complications of an expanding aneurysm, and I think of an aortic dissection as well, are the following:

Answer 3

1) rupture –> exsanguinations (the worst)
2) dilation of the aortic root –> AR
3) rupture into pericardium –> pericardial tamponade
4) rupture into pleura –> hemothorax
5) occlusion of great vessels off aorta –> stroke, others
6) Disruption of radicular arteries supplying the anterior spinal cord (from aneurysm rupture/dissection, surgical stenting or rupture) –> paraplegia
7) compression of proximal structures: trachea/bronchia (difficult intubation or ventilation), SVC (SVC syndrome), left RLN (hoarseness)

Question 4

Major risks of Endovascular Repair of Aortic Aneurysm

Answer 4

1) Many of the same risks that you have from an expanding aortic aneurysm, or aortic dissection or rupture. makes sense
- Hemodynamic instability and massive blood loss are two of these obvious risks
2) Paraplegia - from radicular artery disruption (arteries for anterior spinal cord)
3) Postoperative AKI - big one. Even in the absence of aortic cross-clamping (which is NOT required during endovascular repair), acute postoperatie AKI may occur secondary to:
- pre-operative CKD (common)
- contrast dye during procedure
- Hypoperfusion of kidneys due to: aneurysmal/surgical/stent disruption of the renal arteries, induced hypotension during device deployment, temporary aortic occlusion when sealing the proximal and distal ends of the aortic graft to the aortic wall, significant blood loss, or emboli to renal arteries
4) Visceral/mesenteric injury 2/2 SMA or Celiac A injury, as well as hypotension from blood loss and hemodynamic instabilty
5) Stroke - 2/2 embolization of air or throobmotic material, or HoTN
6) Airway complications - 2/2 aneurysmal compression of trachiea or lung, or other nearby structures
7) possible conversion to open if rupture, stent migration, or other surgical complications
8) ENDOLEAK - resulting in pressurization of the aneurysm with possible enlargement and/or rupture
9) Post-implantation syndrome - 2/2 endotheliala activation by the endoprosthesis

Question 5

Preoperative medical treatment for aneurysm prior to surgery?

Answer 5

The physiologic goal to medical optimization of aortic aneurysm is to reduce the shear pressure which reduces aortic wall stress, which reduces the risk of aneurysmal propagation and dissection or rupture. This is accomplished by reducing the HR and blood pressure. However, you have to be careful in lowering the HR and BP in two main ways:
1) If you drop BP with a vasodilator PRIOR to adequate beta-blockage (ie, i think prior to decreasing the frequency and force of ventricular contracts which decreases wall stress), the aneurysm could rupture 2/2 increased aortic wall stress.
2) Dropping the BP with a vasodilator could lead to inadequate perfusion to end organs –> spinal cord, myocardium, kidneys, mesentary.

So the way to achieve BP and HR control in these aortic aneurysm pts prior to surgery is the following:
1) correct the obvious stuff that may be causing tachycardia and HTN - treate pain, infection, hypovolemia, anemia
2) Utilize short-acting BB’s (esmolol), and once adequate beta blockade was achieved,
3) administer a vasodilator such as nitroprusside.

Question 6

Methods for Spinal Cord Preservation in Aortic Surgery, whether it’s Endovascular (no cross clamp) or Open (yes aortic cross clamp) repair of an aortic aneurysm

Answer 6

1) CSF Drain
2) Passive hypothermia (32-34)
3) avoidance of intraoperative HoTN
4) maintenance of normal Hgb and PaO2
5) neurophysiologic monitoring - SSEP’s and MEP’s usually
6) avoidance of Hyperglycemia
7) Surgeon finding and preserving blood flow through critical intercostal arteries (so reattaching them to either the aortic graft or some other major vessel)
8) Pharmacological intervention: corticosteroids, naloxone, dextrorphan, magnesium, intrathecal papaverine, naloxone, and CCB’s

Question 7

CSF Drain for Endovascular Aortic Aneurysm Repair

Answer 7

CSF drains aren’t just for open aortic surgery cases where there are cross-clamps. They are also for endovascular surgery cases where there is no cross-clamping the aorta, cuz there’s still things that mess with blood flow.

a Lumbar Drain (CSF drain) reduces intraoperative and postoperative CSF pressures, which increases spinal cord perfusion because SCPP = MAP - ISP/ICP/CVP (Spinal Cord Perfusion Pressure = Mean Arterial Pressure - IntraSpinal Pressure or IntraCranial Pressure or Central Venous Pressure).

Target CSF pressure for the lumbar/CSF drain is 8-10 mmHg.

It’s a Class I recommendation to place a CSF drain for those at increased risk for neurologic injury who are undergoing aortic surgery like this, and I think a lot of patients are at risk, even if it’s just the risk of a big surgery itself (like repair of a Crawford Type II thoracoabdominal aneurysm).

Question 8

Risks of CSF/Lumbar Drain Placement

Answer 8

There are obvious risks to placement that must be weighed:
1) Spinal/epidural hematoma
2) headache
3) intracranial bleeding (2/2 tearing of cerebral bridging vessels)
4) Meningitis
5) chronic CSF leakage

THEREFORE, ensure there are no signs of coagulopathy prior to placement of the drain, and monitor the pt postoperatively for development of complications relate to drain placement!

Question 9

What is an endoleak

Answer 9

an endoleak is the failure to completely isolate the aortic aneurysmal sac from arterial blood flow. it’s concerning because the potential for pressurization of the aneurysmal sac (endotension) leading to aneurysm enlargement and rupture.

Question 10

Describe the five types of endoleaks

Answer 10

Type I Endoleak: failure of the seal between the stent-graft and the aortic wall at the proximal or distal attachment site
Type II Endoleak: retrograde flow from the intercostal arteries results in filling of the aneurysm sac
Type III Endoleak: structural failure of the stent-graft results in flow into the aneurysmal sac (usually results with inadequate overlap and seal between modular components of the graft).
Type IV Endoleak: secondary to excessive porosity of the graft itself
Type V Endoleak: describes a situation in which pressurization of the aneurysmal sac occurs despite the absence of an identifiable leak on imaging

Type II and IV Endoleaks: usually benign and rarely require intervention (though type II endoleaks may lead to aneurysm enlargement)

Type I and III Endoleaks: require URGENT intervention since they are associated with increased risk of aneurysmal rupture

Type V Endoleaks: also require intervention of they lead to aneurysmal expansion

Question 11

Is Neuraxial anesthesia ok for a big, long endovascular aortic repair case?

Answer 11

for some SMALLER cases, Neuraxial anesthesia IS acceptable, as long as there are no contraindications such as coagulopathy. However pt must understand that periods of HEAVY sedation would NOT be an option since periodic breath-holding is required during angiography!

For BIG cases - NO. Neuraxial is NOT appropriate. For the following reasons:
1) because during stent deployment you need a MOTIONLESS FIELD ( pause vent + temporary cessation of blood flow in the thoracic aorta may be provided using adenosine or inducing Vfib)
2) there’s a relatively high risk of conversion to open surgery (2/2 to the flatout complexity of some cases)
3) it would preclude the use of neuromonitoring (SSEP’s or MEP’s) to monitor spinal cord perfusion).
4) It would preclude the use of TEE

Question 12

Where should you place A-line for most aortic endovascular repair surgeries?

Answer 12

RIGHT RADIAL artery usually, as both femoral arteries and the Left brachial artery are often utilized for access during the procedure.

Question 13

Should you get a PRE-induction A-line

Answer 13

obviously yes. You must NOT let BP get too high so that aneurysm or dissection doesn’t propogate. And they probably have CAD and other things where HoTN (inadequate diastolic BP for coronary filling in CAD) would be bad too

Question 14

Surgeon Requests a hemodynamically “still” field for endograft deployment. How do you accomplish this?

Answer 14

A “motionless field” is required for endovascular repair of the ASCENDING aorta, aortic ARCH, or PROXIMAL DESCENDING descending aorta, which is accomplished by any of the following:
1) Adenosine 6-12mg via central line –> transient AV block
2) Transvenous pacing at 150-180 bpm –> decreased LV preload, SV, and CO
3) Right atrium flow occlusion - achieved by balloon through femoral or jugular vein into right atrium to inflate in the IVC or SVC

for NEWER self-expanding aortic endografts in aortic areas NOT mentioned bove, they only require temporary reduction in CO during stent deployment - MAP 60-70 mmHg nad HR 50-60 bpm suffices

Question 15

What is the rationale for a hemodynamically “still” field while deploying an aortic graft?

Answer 15

1) Once deployed, repositioning of most thoracic endografts is difficult to impossible. You only have one shot, so must eliminate all movement/variables so get it right the first time.

2) Because of the proximity of major vessels originating form the aorta to the proximal and distal landing fields of thoracic and aortic arch stent-grafts, stent migration or encroachment would potentially be catastrophic.

3) The high volume of blood flow in teh thoracic aorta can lead to a “windsock effect”, pulling even a perfectly deployed graft distally before complete deployment is achieved. So you eliminate the windsock effect by decreasing blood flow temporarily.

Question 16

How do you provide RENAL PROTRECTION during ENDOVASCULAR Aortic Surgery Repair?

Answer 16

Multiple Strategies for RENAL PROTECTION during Endovascular aortic aneurysm repair where CONTRAST-DYE is often given. Here’s what to do:

Things I can do as the Anesthesiologist:
1) Adequate hydration (caution IVF though in CHF and such)
2) Try to use TEE whenever possible in lieu of contrast dye
3) NaHCO3- (Sodium Bicarbonate) infusion!
4) Antioxidants - eg, N-acetylcysteine (NAC, mucomyst) or ascorbic acid. However, the NAC can cause anaphylactic reactions and is NOT universally recommended d/t insufficient evidence.
5) Avoid nephrotoxic drugs - ACEi’s, ASA, NSAIDs, aminoglycosides
6) Give Renal Protective Drugs:
- Statins (preserved renal function after surgery requiring suprarenal aortic cross-clamping)
- Mannitol (12.5-25 g/70kg or 0.25 g/kg, administered BEFORE cross-clamp) - increases renal cortical blood flow, is a free radical scavenger, increases renal prostaglandin synthesis, decreases rennin secretion, and reduces ischemia-induced cellular edema
- Loop diuretics (less effective than mannitol)
- Low-dose Dopamine (1-3 mcg/kg/min) - loop diuretics and dopamine may provide protection through increased renal blood flow and increased urine output
- Fenoldopam - a selective dopamine agonist that preferentially dilates the renal and splanchnic vasculature
With all these meds however (mannitol, loop diuretics, low-dose dopamine, and fenoldopam), there is LITTLE EVEIDENCE that they actually improve outcome following aortic surgery

Things SURGEON can do:
1) Use contrast dye that is NON-ionic, low or iso-osmolar, and low in viscosity

Question 17

Something went wrong during vascular sheath advancement for deploying the aortic endograft - surgeon ruptured the femoral artery during this process. So now he needs to CONVERT TO OPEN surgery and repair the artery using a “clamp and sew” technique (no bypass). How would you provide RENAL PROTECTION during the aortic aneurysm repair?

Answer 17

“Clamp and Sew” is where the aorta was clamped proximally and distally to the diseased segment, and a graft sewn into the intervening segment. This is, essentially, “Cross-clamping” I think. Cross-clamping is obviously only a thing in OPEN surgery, since belly has to be open in order to access the aorta for cross-clamping.

Ways for RENAL PROTECTION during OPEN (CROSS-CLAMPING) Aortic Repair:

Things I can do as the anesthesiologist:
1) Maintain adequate intravascular VOLUME / hydration during cross-clamping - this reduces the requirement for active (think ATP or energy expenditure) reabsorption of salt and water in the kidneys, thereby reducing medullary oxygen requirements, ischemia, and perioperative renal dysfunction
2) Maintain Hemodynamic stability during cross-clamping

Things SURGEON can do:
1) minimize cross-clamp time (lol, good luck telling surgeon)
2) PRE-CONDITIONING, with intermittent cross-clamping of the internal iliac arteries prior to aortic cross-clamping
3) Distal aortic perfusion (i think by a shunt?)
4) Systemic and/or regional HYPOTHERMIA - the latter may be achieved with the direct instillation of renal preservation fluid into the renal artery using cold LR at 4 deg C.

Question 18

What if, instead of a SUPRArenal cross clamp, the aortic cross-clamp was INFRARENAL? What renal protective strategies would you employ?

Answer 18

you would STILL provide the same renal-protective strategies for open cross-clamping - Even with aortic clamping below the renal arteries, there is STILL a decrease in renal blood flow (up to 40% 2/2 alterations of the RAAS and vasoconstriction) and a deleterious redistribution of intra-renal blood flow to the cortex (so I think away from the medulla in the middle and more blood flow just to the cortex in the periphery).

Other contributing factors to renal injury even when XC is INFRArenal are 1) direct surgical trauma to the renal arteries, and 2) embolization of atherosclerotic debris to the kidneys.

Question 19

Cross-clamping of the aorta - list the physiologic affects. In this case, say the XC was supraceliac

Answer 19

First off, XC effects are more extreme as you clamp higher up on the aorta. once the XC is INFRArenal, there are MINIMAL hemodynamic changes. Other factors that affect the CV response to XC are XC duration, volume status, LV fxn, and use of distal bypass.

Here are the effects of cross-clamping:
1 . Increased arterial blood pressure above the level of the clamp
2. Increased coronary artery blood flow
3. Increased left ventricular wall stress
4. Increased central venous pressure
5. Increased pulmonary artery wedge pressure
6. Decreased arterial blood pressure below the clamp
7. Decreased cardiac output - not as intuitive as others. Think ↑ afterload (causing ↓ CO) is more significant that ↑ preload (which ↑ CO). And UBP says that CO might decrease, stay the same, or increase depending on variances in preload, afterload, and cardiac contractility.
8. Decreased renal blood flow

Metabolic consequences of XC aorta:
1. Decreased total-body oxygen consumption
2. Decreased total-body carbon dioxide production
3. Increased mixed venous oxygen saturation
4. Decreased total-body oxygen extraction
5. Increased epinephrine and norepinephrine
6. Respiratory alkalosis
7. Metabolic acidosis

There’s also increased CSF pressure, which is a good reason for a lumbar drain. The increased systemic pressure proximal to the clamp results in redistrubiton of blood to the intracranial compartment, with subsequent redistribution of CSF to teh spinal fluid space, whihc increases the intrathecal CSF pressure or ISP.

Question 20

What are the beneficial effects of hypothermia during this surgery?

Answer 20

Class IIa recommendation: Both systemic and regional hypothermia have can limit ischemic injury the the spinal cord and kidneys. Hypothermia decreases cerebral and spinal cord O2 requirements by 5% for each 1 degree decrease below 36 deg Celcius

Risks associated with induced hypothermia:
- Cardiac arrhythmias (Afib or Vfib)
- Myocardial depression
- Increased metabolic oxygen requirements 2/2 shivering
- coagulopathy

If cross-clamping the aorta (“clamp and sew” technique) and NOT utilizing bypass, then cooling via extracorporeal circulation (any time blood taken out of patient and processed by a machine [eg, bypass] then returned to patient). In that case, could cool the patient to 30-34 degrees with passive cooling, nad consider utilizing regional hypothermia which involves an EPIDURAL infusion of 4 deg C saline and/or direct instillation of cold RENAL preservation fluid into the renal artery (using cold LR).

Question 21

The patient who is getting this AAA repair has CAD. We’ve established that unfortunately we’re converting from endovascular repair to open, so surgeon will have to cross-clamp the aorta. What are your overall hemodynamic goals during XC?

Answer 21

Proximal to clamp: REDUCE AFTERLOAD enough to avoid cardiac ischemia, while at the same time maintaining adeuate perfusion of the coronaries. If pressure gets too high (too high of afterload) you may see some ST depressions and need vasodilators (esmolol, SNP, NTG, nicardipine, clevidipine) and may even need surgeon to release clamp

DISTAL to clamp: maintaining ADEQUATE PERFUSION to tissues to avoid ischemic injury. may require temporary SHUNT or initial PARTIAL BYPASS to improve distal perfusion

Question 22

One vasodilator you might use to reduce proximal afterload is SNP (sodium nitroprusside). Explain the possible toxicity

Answer 22

when SNP enters an RBC, a nonenzymatic rxn results in release of NO (nitric oxide) and cyanide ions. the cyanide ions can:
1) react with metHgb (methemoglobin) to form cyanmethemoglobin
2) react with thiosulfate to form thiocyanate
3) bind to tissue cytochrome oxidase, which impairs normal tissue oxygen utilization

The impaired O2 utilization leads to cyanide toxicity, characterized by metabolic acidosis, increased venous O2 content, cardiac arrhythmias, and tachyphylaxis.

The risk of developing cyanide toxicity is minimal when using doses less than 0.5 mg/kg/h.

Question 23

How do you treat acute Cyanide Toxicity?

Answer 23

1) Discontinue the SNP infusion! Don’t forget to actually say this
2) 100% O2
3) Sodium Thiosulfate - provides substrate for the cyanide ions to form thiocyanate
4) Amyl nitrate or Sodium nitrate - both oxidize hemoglobin to methemoglobin, thereby increasing the subtrate for metHgb to bind cyanide to form cyanmethemoglobin
5) Hydroxocobalamin - combines with cyanide ions to form cyanocobalamin (aka Vit B12)

Basically, all the drugs above result in chemical reactions that effectively remove excess cyanide ions from circulation, so they are unavailable to react with tissue cytochrome oxidase

Question 24

How do you prepare for the release of the cross-clamp?

Answer 24

1) decrease depth of anesthesia
2) administer vasodilator to facilitate VOLUME LOADING. Eg NTG, SNP
3) utilize TEE and/or PA catheter to guide volume loading and aid in rapid identification and tx of hemodynamic instability
4) discontinue any vasodilators just prior toXC release (including those utilized to assist volume loading)
5) correct any electrolyte abnormalities, acid-base disturbances, or coagulopathy
6) have inotropes and vasopressors available to treat any sustained reduction in SVR following XC release
7) ask teh surgeon to release the XC gradually, allowing sufficient time for physiologic compensation and/or medical intervention

Question 25

How do you treat HYPOtension after XC release?

Answer 25

You do everything:
1) FLuid bolus - lines wide open
2) Vasopressors
3) Trendelenburg
4) re-apply XC
5) decrease anesthetic depth
6) volume load - now definitely withOUT vasodilators
7) re- release XC after you’ve got HoTN under control, but now SLOWLy to allow for physiologic compensation

identify all the OTHER potential causes of hypotension: hemorrhage (low filling pressures, obvious bleeeding on field), arrhythmia, anesthetic-induced, myocafdial ischemia (WMA on TEE, EKG changes, elevated filling pressures), Tension PTX, acid-base disturbance, citrate-induced hypocalcemia, and hypothermia)

Question 26

How does cross-clamping kill the kidneys?

Answer 26

XC of the aorta, even when infrarenal, is associated with increased renal vascular resistance, decresaed renal perfusion, decreased renal cortical blood flow, and acute renal failure - it’s almost always ATN (Acute Tubular necrosis)

contrast media exposure is directly cytotoxic to kidneys, enhances cellular damage caused by ROS, and increases renal vascular resistance

So overall, postoperative renal failure is caused by renal ischemia, nephrotoxins, air embolization, or activation of the RAAS

Risk factors for renal failure when XC surgery:
1) advanced age
2) prolonged XC time
3) cardiac disease
4) pre-existing renal disease

Question 27

What is post-implantation syndrome?

Answer 27

Post-implantation syndrome is a post-operative complication associated with endovascular aortic aneurysm repair, thought to occur secondary to endothelial activation by endoprothesis. The syndrome, which is characterized by fever, elevated inflammatory mediators, and leukocytosis, is usually mild and self-limited (lasting 2-10 days). While treatment often involves NSAIDs, I would avoid administering if a patient has renal failure.