Download Anesthesia for Thoracic Aortic Aneurysm Endovascular Stenting

Maged Argalious, MD and Katja R. Turner, MD
Anesthesia for Thoracic Aortic Aneurysm
Endovascular Stenting
Key Words:
Endovascular aortic stent graft, cerebrospinal fluid drainage, endoleaks
Stem Case and Key Questions:
A 76 years old male, 89 kg, 1,7m presented to the emergency department with an
acute onset of chest pain radiating to the back.
His medical history was significant for coronary artery disease, hypertension and
chronic renal insufficiency as well as an abdominal aortic aneurysm repair 7 years
earlier.
He had undergone two coronary artery bypass graft surgeries 14 and 6 years prior
to this presentation. In the emergency department, aspirin and intravenous beta
blockers were initiated, his chest pain only partially resolved and a 12 lead EKG as
well as cardiac enzyme tests were negative for acute myocardial injury. The next
day, a dobutamine stress echocardiography (DSE) revealed evidence of reversible
ischemia in the inferior segments of the myocardium as well as scarring in the
anterolateral basal segment. His left ventricular ejection fraction was estimated at
42%. Despite of sub-optimal picture quality of his aorta during the DSE, a
suspicion of aneurysmal dilatation of his descending thoracic aorta prompted
further workup with a CT can of the chest and abdomen revealing a 6.5 cm
thoracic aortic aneurysm. A cardiac catheterization revealed severe native triple
vessel disease, patent grafts to the left anterior descending artery, the posterior
descending artery and the lateral circumflex, but occluded saphenous vein grafts to
the right coronary artery and 1st diagonal artery. An episode of ventricular
tachycardia during his hospitalization prompted insertion of an automatic
implantable cardioverter defibrillator (ICD).
The patient also had a documented 75% right subclavian artery stenosis as well as
chronic obstructive pulmonary disease with an FEV1 65% of predicted and an
FEV1/ FVC 68% of predicted.
Key Questions:
1.Is a conservative medical approach a valid option in this patient?
2. What are the therapeutic options in this patient?
3. Do you agree with the described diagnostic approach in this patient?
4. Which TEE views are useful in the diagnosis and intraoperative monitoring of
thoracic aortic aneurysms?
2. What are the therapeutic options in this patient?
3. Do you agree with the described diagnostic approach in this patient?
4. Which TEE views are useful in the diagnosis and intraoperative monitoring of
thoracic aortic aneurysms?
5. What anesthetic technique would you use for this patient?
6. Would you deactivate the AICD prior to any surgical procedure?
7. What are the hazards of central venous monitoring in this patient?
8. Which artery are you planning to use for intra-arterial monitoring?
Case:
The decision was made to proceed with thoracic aneurysm endovascular stenting.
On the day of surgery, the patient was sedated with 1 mg of intravenous
midazolam.
After application of transthoracic defibrillator pads, the ICD was turned off using
an external deactivating device.
In addition to standard ASA monitors, a left radial arterial catheter was placed
under local anesthesia.
Using the sitting position, an L3-4 intrathecal catheter was inserted utilizing an
18G Tuohy needle.
The intrathecal catheter was bolused with 10mg of hyperbaric bupivacaine 0.75%
and 0.2 mg of epinephrine in addition to 15 ug of fentanyl.
In the Trendlenberg position, an 8.5 F right internal jugular Swan Ganz introducer
was placed under local anesthesia, utilizing fluoroscopy to track the guidewire
insertion and avoid dislodgement of the recently introduced ICD leads.
In addition, a 14 G peripheral I.V. was inserted in the right cephalic vein.
After confirmation of adequate anesthesia (T8 sensory level), the surgeons
performed a diagnostic arteriography through the right femoral artery, which
confirmed the preoperative finding of a large descending thoracic aneurysm. The
left femoral artery was then exposed, but repeated attempts at insertion of the
endograft under fluoroscopy through the left femoral artery were unsuccessful due
to a small iliofemoral diameter.
The right femoral artery was subsequently exposed, and the endograft was
successfully inserted through the introducer sheath. After repeated failed attempts
at advancing the endograft over the guidewire to the aneurysm site due to
tortuosity of the thoracic aorta, the surgeon proceeded to access the left brachial
artery.
The right femoral artery was subsequently exposed, and the endograft was
successfully inserted through the introducer sheath. After repeated failed attempts
at advancing the endograft over the guidewire to the aneurysm site due to
tortuosity of the thoracic aorta, the surgeon proceeded to access the left brachial
artery.
A long guidewire was passed through the left brachial artery to the right femoral
artery and by applying tension on both ends of the guidewire; the endograft was
able to track the guidewire.
The left femoral sheath was used to transduce the systemic arterial pressures
during the period of left brachial artery usage, since flow to the left radial artery
was interrupted during that time.
Due to interference of the external defibrillator pads with fluoroscopic
identification of the exact site of the endograft during its advancement to the
thoracic level, the site of the anterior defibrillator pad was switched to the left
axilla.
Following successful introduction of the endograft to the thoracic aorta, and prior
to its deployment, the patient sustained an episode of nausea followed by an acute
reduction of blood pressure to a systolic of 70 mmHg (baseline 160 mmHg). This
was accompanied by a rise in heart rate and a drop in central venous pressure.
Key Questions:
1.What is you differential diagnosis for hypotension, tachycardia and a low central
venous pressure?
2. What hemodynamic parameters are desirable during the period of stent
deployment?
Case:
The surgeons were notified and aneurysm rupture was initially suspected, but after
blood started to trickle on the surgeon s shoes, it was discovered that the left
femoral sheath had been accidentally pulled out from the left femoral artery
leaving a hole that continued to bleed under the drapes.
This episode resulted in an estimated blood loss of 600cc.
The left femoral artery was temporarily clamped and the femoral sheath
reintroduced, the patient was fluid resuscitated and reassured, and baseline
hemodynamics were restored.
During deployment of the stent, an esmolol infusion was started and was titrated to
a MAP of 50-60mmHg. The patient was asked to hold his breath for a few seconds
while the endograft was deployed. Successful deployment was confirmed by a
repeat arteriography, the patient was transferred to the recovery unit, where his
intrathecal catheter was utilized for CSF drainage to a pressure of 10 mmHg for
the next 72 hours. The transthoracic defibrillator pads were removed once the ICD
During deployment of the stent, an esmolol infusion was started and was titrated to
a MAP of 50-60mmHg. The patient was asked to hold his breath for a few seconds
while the endograft was deployed. Successful deployment was confirmed by a
repeat arteriography, the patient was transferred to the recovery unit, where his
intrathecal catheter was utilized for CSF drainage to a pressure of 10 mmHg for
the next 72 hours. The transthoracic defibrillator pads were removed once the ICD
was reactivated.
Neurologic examination for evidence of sensory or motor deficits was performed
every 4 hours for the subsequent 48 hours. The patient was discharged home after
his cardiologists recommended medical treatment of his coronary artery disease,
due to the technical difficulty in stenting his occluded vein graft to the right
coronary artery, and the absence of distal target sites even if a third coronary artery
surgery was considered.
Key Questions:
1.Is cerebrospinal fluid drainage indicated in thoracic aneurysm stenting?
2. What are considerd to be risk factors for spinal cord ischemia during thoracic
endovascular stent placement?
3. What is the rationale for CSF drainage? What is the therapeutic end-point?
4. What other spinal protection strategies are feasible in cases of thoracic
aneurysm stenting?
5. Do you agree with this choice of anesthetic?
6. Do you agree with the choice of monitoring?
7. What adjuvant medications should be prepared during aortic aneurysm stenting?
8. What are the side effects of adenosine? Is there an antidote?
9. How do renal protective strategies differ in cases of endovascular stenting
versus open repair?
10. What is postimplantation syndrome? What are the complications of
endovascular aneurysm stenting?
11. What is endotension? What is endoleak ? What are the types of endoleaks?
Discussion:
Untreated patients with large (more than 5 cm) thoracic aneurysms have a 2 year
mortality rate >70%.
In this patient, the ongoing chest pain radiating to the back is a signal for a
possible contained rupture of the aneurysm, making early intervention even more
necessary.
Untreated patients with large (more than 5 cm) thoracic aneurysms have a 2 year
mortality rate >70%.
In this patient, the ongoing chest pain radiating to the back is a signal for a
possible contained rupture of the aneurysm, making early intervention even more
necessary.
Open surgical repair on the descending aorta is challenging due to the imminent
risk of high morbidity, including paraplegia, renal failure, stroke and prolonged
ventilatory dependence, and mortality.
Patients who are not candidates for an open repair because of comorbidities may
be treated with endovascular repair.
Although endovascular stenting is still considered a palliative treatment, successful
exclusion of the aneurysm results in a reduction in aneurysm diameter and
prevention of aneurysm rupture.
The presence of ongoing chest pain radiating to the back should alert the treating
physician to the possibility of other etiologies, such as an aortic dissection or an
impending aneurysm rupture.
Dobutamine stress echocardiography is contraindicated in both these conditions. A
CT scan or MRI of the chest, or a Transesophageal echocardiography can reliably
diagnose the presence of an aortic aneurysm or an aortic dissection. A
transthoracic echocardiography may miss the diagnosis of an aortic aneurysm,
especially aortic aneurysms in the region of the descending aorta, due to poor
accoustic access and suboptimal image resolution.
Cerebrospinal fluid drainage theoretically increases spinal cord blood flow by
decreasing CSF pressure resulting in an increased spinal cord perfusion pressure.
Spinal cord perfusion pressure is defined as distal mean aortic pressure minus CSF
pressure.
The blood supply of the spinal cord is made up of 2 posterior spinal arteries and
one anterior spinal artery. The thoracic portion of the anterior spinal artery is
supplied by radicular branches of the intercostal arteries.
The largest of the radicular branches, the artery of Adamkiewicz (arteria
radicularis magna), arises directly from the aorta at T9-T12 in the majority of
cases, but can arise anywhere between T5 and L5. Exclusion of this artery during
aneurysm stenting can result in paraplegia.Other postulated mechanisms are the
occurrence of hypoperfusion as a result of hypotension as well as thrombosis or
embolization of the arteries supplying the anterior spinal artery. The injury seen
after ischemia of the spinal cord (anterior spinal artery syndrome) is manifested by
loss of motor function and pinprick sensation and preservation of vibratory and
position sense. A history of prior aneurysm repair, whether by an open or an
endovascular approach puts patients at increased risk of neurologic damage due to
the limited available collateral circulation of the spinal cord following exclusion of
part of the collateral blood supply by priorinterventions.
The use of cerebrospinal fluid drainage is supported by animal studies indicating a
position sense. A history of prior aneurysm repair, whether by an open or an
endovascular approach puts patients at increased risk of neurologic damage due to
the limited available collateral circulation of the spinal cord following exclusion of
part of the collateral blood supply by priorinterventions.
The use of cerebrospinal fluid drainage is supported by animal studies indicating a
beneficial effect of CSF drainage to a pressure of 10 mmHg. Coselli et al, in a
recent prospective randomized trial demonstrated the usefulness of CSF drainage
and distal aortic perfusion in preventing paraplegia after thoracoabdominal
aneurysm repair (7). Safi et al also reported that delayed paraplegia was reversed
with aggressive CSF drainage after recognition of neurologic deterioration (11). In
addition a recent meta-analysis supported the usefulness of CSF drainage in
preventing paraplegia after thoracocabdominal aneurysm surgery (8). Recent
reports indicate the selective use of CSF drainage in patients felt to be at increased
risk for spinal cord ischemia.(13,14). These risk factors include:
1.Anticipated coverage of T9-12.
2.Coverage of long segments of thoracic aorta.
3.Compromized collateral perfusion (e.g. previous AAA repair).
4. Symptomatic spinal cord ischemia post repair.
In summary, prophylactic CSF drainage is definitely indicated in selective cases of
thoracic aneurysm stenting such as patients with abdominal aneurysm stenting who
had prior long segment thoracic aortic exclusion, due to the limited remaining
collateral blood flow to the spinal cord. It has been show to be therapeutic in new
onset spinal cord ischemia after thoracic endovascular stent placement when
combined with increasing mean arterial pressures.
The use of CSF drainage is not without complications. Overdrainage can result in
neurologic complications such as pneumocephalus, brain collapse, or temporal
downward herniation with kinking of the posterior cerebral artery resulting in an
acute brain infarction or death.Other rare complications such as infection, subdural
hematoma or nerve injuries can occur.
Monitoring motor evoked potentials (MEP) or somatosensory evoked potentials
(SSEP) of the spinal cord during placement of a retrievable stent graft in the
descending thoracic aorta to temporarily interrupt blood flow to the intercostal
arteries can predict spinal cord ischemia after permanent stent placement.
Since sensory monitoring is more likely to detect posterior column ischemia, it
might miss injuries to the anterior column. As a result, paraplegia can occur
despite normal SSEP signals.
Motor evoked potentials have been successfully used to monitor anterior spinal
column ischemia. Stimulation of the motor cortex or the cervical spine with
sensing over the popliteal nerve is the most commonly employed technique. Like
SSEP s, MEP s are affected by inhalational anesthetics and hypothermia.
Glucose containing solutions should be avoided due to the deleterious effects of
glucose on cerebral and spinal cord ischemia.The use of steroids, mannitol and
hypothermia for reduction of neurologic complications has not been studied in
cases of endovascular repair.Their use in cases of open repair (with aortic cross-
SSEP s, MEP s are affected by inhalational anesthetics and hypothermia.
Glucose containing solutions should be avoided due to the deleterious effects of
glucose on cerebral and spinal cord ischemia.The use of steroids, mannitol and
hypothermia for reduction of neurologic complications has not been studied in
cases of endovascular repair.Their use in cases of open repair (with aortic crossclamping) is based on animal data.The use of steroids for spinal cord protection
only showed benefit when combined with CSF drainage.Mannitol has been shown
to reduce CSF volume and brain tissue volume and thereby reduce CSF
pressure.Although animal studies confirm a benefit of mild hypothermia with
aortic crossclamping, clinical reports of epidural cooling have been less successful.
Naloxone has also been reported to reduce spinal cord injury after TAA repair,
especially when combined with CSF drainage. The protective mechanism has been
recently reported to be due to a reduction in the level of excitatory amino acids
(glutamate). Naloxone has not been studied in endovascular aneurysm stenting.
Thoracic aneurysm stenting can be performed under spinal, epidural or general
anesthesia.
Although local anesthesia can be employed, the possibility for utilizing an iliac
artery conduit for stent introduction in cases of insufficient femoral artery diameter
site, with the need for an abdominal incision makes local anesthesia less desirable.
Some centers have reported beneficial effects with the use of regional anesthesia,
e.g. less vasopressor use, shorter ICU and hospital stay. Other studies have
reported equal efficacy and safety when compared to general anesthesia. We
utilize epidural anesthesia in most aneurysm stent cases. If an intrathecal catheter
for CSF drainage is required, the intrathecal catheter can also be utilized for spinal
drug delivery, making sure to avoid drainage of CSF for 30 minutes thereafter. The
use of general anesthesia is limited to patients on anticoagulants or if other
contraindications to regional anesthesia exist.
The use of intraartrial pressure monitoring is mandatory. In addition to the ever
present risk of aneurysm rupture and the potential for massive blood loss, these
patients’ co-morbidities dictate a continuous monitoring technique. More
importantly, the possibility for the use of hypotensive agents during stent
deployment makes an intraarterial catheter indispensable. For thoracic stenting
procedures in particular, the site of arterial cannulation has to be discussed with the
surgeon, since they may utilize the right or left brachial artery during the
procedure. Although the right radial artery is farthest away from the aneurysm site
in our case, the presence of a right subclavian artery stenosis will underestimate
the true aortic pressures and should therefore be avoided.
In cases with a recent ICD or pacemaker insertion (less than 6 weeks), the risk of
lead dislodgement during central line insertion is real. Due to the development of
fibrosis around the leads, this risk tapers off after 6 weeks.
The options for central line insertion are either to insert it under fluoroscopic
guidance, to cannulate the external jugular vein to avoid central venous
monitoring altogether.The use of hypotensive infusions during stent deployment
makes central line insertion desirable.Even though central venous pressures are a
fibrosis around the leads, this risk tapers off after 6 weeks.
The options for central line insertion are either to insert it under fluoroscopic
guidance, to cannulate the external jugular vein to avoid central venous
monitoring altogether.The use of hypotensive infusions during stent deployment
makes central line insertion desirable.Even though central venous pressures are a
resultant effect of intravascular volume, intrathoracic pressure and right ventricular
function, the sudden drop in central venous pressure can help identify acute
hypovolemia secondary to bleeding, especially that blood loss is usually occult in
endovascular cases.
In cases of abdominal aortic aneurysm stenting, especially in relatively healthy
patients and in centers with established surgical expertise, large bore peripheral
intravenous access may negate the need for central access.
In patients with ICD, the indication for insertion has to be identified. Deactivation
of the ICD prevents its inappropriate triggering during the procedure; especially
that slowing of the heart with intravenous adenosine in some cases will result in
the occurrence of bradyasystole. The use of transthoracic defibrillator pads during
the period when the ICD is deactivated ensures the most rapid defibrillation in case
of occurrence of ventricular tachycardia or fibrillation.
During stent deployment the surgeons require a motionless field, since motion
might lead to stent migration or encroachment of the stent on major vessels
originating from the aorta (celiac, superior mesenteric).To achieve a motionless
field, some centers utilize adenosine in a dose of 6-12 mg, causing a transient
atrioventricular heart block. Mild sedation of patients done under regional
anesthesia is necessary prior to intravenous adenosine, since its side effects: facial
flushing, dyspnea, chest tightness, and bronchospasm, can cause patient
discomfort. The pharmacological effects of adenosine can be antagonized by
methylxanthines (theophylline).With the advancement of endovascular technology
and surgical expertise, most surgeons only require a modest slowing of heart rate (
50-60 beats/min ) as well as a reduction in mean arterial pressure (60-70 mmHg)
during endovascular stent deployment.
This can be most easily achieved with the use of infusions of short acting
medications such as esmolol or sodium nitroprusside.Unlike cases of open repair
of aneurysms, where ischemia from aortic cross-clamping is the main etiology of
postoperative renal dysfunction, the etiology of renal dysfunction in cases of
aneurysm stenting is mainly related to the intravenous dye injected during
aneurysm stenting.
Other etiologies such as emboli to the renal arteries, hypoperfusion as a result of
hypotension, or mechanical encroachment of abdominal stents on the origin of the
renal arteries are possible etiologies. Preoperative renal dysfunction is a major risk
factor in the occurrence of postoperative renal failure. Acetylcysteine has been
shown to reduce the incidence of radiographic contrast agent induced renal failure.
It should be started 48 hours prior to the anticipated intravenous dye load. The
maintenance of euvolemia and avoidance of hypotension to preserve the renal
perfusion pressure are still cornerstones in the successful perioperative renal
protection.
shown to reduce the incidence of radiographic contrast agent induced renal failure.
It should be started 48 hours prior to the anticipated intravenous dye load. The
maintenance of euvolemia and avoidance of hypotension to preserve the renal
perfusion pressure are still cornerstones in the successful perioperative renal
protection.
Postimplantation syndrome is the transient elevation of body temperature and Creactive protein levels, and mild leucocytosis that occurs several hours following
deployment of the endovascular stent. The lack of knowledge for this physiologic
entity might lead to unnecessary interventions.
Early complications of stenting include renal failure, bowel infarction, lower
extremity embolism, false lumen rupture, and paraplegia.
Delayed complications of stenting include stent graft fracture, stent graft migration
or prolapse into the aneurysm, stent graft infection, stent graft leakage, and
expansion and rupture of the treated aneurysm.
Endotension is the continued aneurysm enlargement without detectable endoleak
and may be due to limits of imaging technology or transmission of thrombus or
graft.
Endoleak is the occurrence of blood flow into the lumen of the aneurysm, but
outside the endovascular graft.
Endoleak has its own classification system:
Type I: occurs from the attachment sites at the proximal or distal ends of the graft.
Type II: occurs from branches off the excluded portion of the vessel, essentially
back bleeding from tributaries that have not thrombosed following aneurysm
exclusion.
Type III: occurs from module disconnection or fabric tear.
Type IV: occurs through intact, but porous, fabric.
While types II and IV are considered benign, especially if not associated with an
increase in aneurysm diameter, types I and III require interventions such as
placement of extension cuffs or even open surgical treatment.
Type I
Type II
Type III
Type IV
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