Aortic aneurysm dr jeevraj

Aortic aneurysm
• Aortic aneurysm is a localized or diffuse dilation of an aorta
with a diameter at least 50% greater than the normal size
of the aorta
• Aneurysm is the second most frequent disease of the aorta
after atherosclerosis
• The strongest predictor of AAA formation is positive family
history
• Smoking is the most important modifiable risk factor in the
formation, progression, and rupture risk of AAA
• The male to female ratio is approximately 2:1, although
women have a higher incidence of aneurysm rupture.
• mean age for diagnosis in sixth decade of life

Type
• Abdominal Aortic aneurysm
• Thoracic aneurysms
• Thoraco-Abdominal Aortic aneurysm
•
• 45% of thoracic aneurysms involved the
ascending aorta, 10% the arch, 35% the
descending aorta, and 10% the thoracoabdominal
aorta

Classification by shape
Fusiform aneurysms are more common,
associated with atherosclerotic or collagen
vascular disease, and usually affect a longer
segment of the aorta, producing a dilation of the
entire circumference of the vessel wall.
Saccular aneurysms are more localized, confined
to an isolated segment of the aorta, and produce
a localized outpouching of the vessel wall
Aortic arch aneurysms are commonly saccular
Fusiform aneurysms have a higher operative
mortality than saccular aneurysms

ETIOLOGY
 atherosclerosis,
 cystic medial necrosis,
syphilitic aortitis
Marfan’s
Type IV Ehlers-Danlos
Infection (syphillis)
Arteritis (giant cell, Takayasu, Behcet’s)

Risk Factors
– Smoking
– COPD
– HTN
– Male gender
– Older age
– High BMI
– Abnormal aortic valve (e.g., bicuspid valve)
– Family history

pathophysiology
• The number of collagen and elastic fibres is reduced
within the aneurysmal segment of the aorta vascular
wall strength is further compromised by several factors
(i) local elastin resorption caused by increased elastase
activity;
(ii) localized wall inflammatory changes;
(iii) increased protease activity;
(iv) mural thrombus formation in the arterial wall and
plasminogen activation

Ruptured AAA
Die outside
Hospital
Die In Hospital
Survive with
major
complications
Survive with
minor or no
complication
• Triad of
 Abd. or back
pain
 Hypotension
 Pulsatile
Abd. mass

Aortic growth in thoracic aortic
aneurysms
• Familial TAAs grow faster, up to 2.1 mm/year (combined ascending
and descending TAA).
• Syndromic TAA growth rates also vary.
• In patients with Marfan syndrome, the TAA growth is on average at
0.5–1 mm/year, whereas TAAs in patients with Loeys-Dietz
syndrome (LDS) can grow even faster than 10 mm/year, resulting in
death at a mean age of 26 years.
• TAAs of the descending aorta grow faster (at 3 mm/year) than
those in ascending aorta (1 mm/year)

Complications of Thoracic
Aortic Aneurysms
• Aortic rupture
• Aortic regurgitation
• Tracheobronchial and esophageal compression
• Right pulmonary artery or right ventricular
outflow tractobstruction
• Systemic embolism from mural thrombus

Risk of aortic dissection
• There is a rapid increase in the risk of
dissection or rupture when the aortic
diameter is 60 mm for the ascending aorta
and 70 mm for the descending aorta.
• Although dissection may occur in patients
with a small aorta, the individual risk is very
low

In Marfan syndrome, aortic enlargement is
generally maximal at the sinuses of Valsalva,
responsible for annulo-aortic ectasia.
 In patients with BAV, three enlargement
patterns are described
 Level of the sinuses of Valsalva,
Supracoronary ascending aorta,
The sinotubular junction level (cylindrical
shape).

Natural History
0
5
10
15
20
25
<2.75
cm/m2
2.75-4.25
cm/m2
>4.25
cm/m2
Aortic Size Index (ASI)
AnnualRiskofRupture
ASI = aortic dia (cm)/body surface area (m2)

SYMPTOMS
• Most of aortic ANEURSYMS may be clinically silent.
• Anterior chest pain secondary to compression of
• (1) Coronary arteries
• (2) Sensory mediastinal nerves
• Chronic back pain may occur descending aortic aneurysms
• CHF symptoms secondary to aortic annular enlargement
• (1) Widened pulse pressure
• (2) Diastolic murmur
• Facial and upper trunk venous congestion secondary to
superior vena cava compression
• Blood pressure usually elevated chronically

Conti .
Acute deep, aching or throbbing chest or abdominal pain that
can spread to the back, buttocks, groin or legs, suggestive
of AD or other AAS, and best described as ‘feeling of
rupture’.
 Cough, shortness of breath, or difficult or painful
swallowing in large TAAs.
 Constant or intermittent abdominal pain or discomfort, a
pulsating feeling in the abdomen, or feeling of fullness after
minimal food intake in large AAAs.
 Stroke, transient ischaemic attack, or claudication
secondary to aortic atherosclerosis.
 Hoarseness due to left laryngeal nerve palsy in rapidly
progressing lesions

Aortic Aneurysms
Diagnosis
• Arteriography:
– Cannot determine aneurysm size because of mural
thrombus
– Indications for obtaining arteriography
• Suspicion of visceral ischemia
• Occlusive disease of iliac and femoral arteries
• Severe HTN, or impair renal function
• ? Horseshoe Kidney
• Suprarenal of TAAA component
• Femoro-Popliteal Aneurysms

CHEST XRAY
• Loss of aortic contour
• Mediastinal widening
• Dilated descending thoracic
aorta,
• aortic calcifications
• upward deviation of the left
mainstem bronchus, and/or
new left pleural effusion.
• Deviation of the trachea to the
right
• Left hemothorax

Aortic Aneurysms
Diagnosis
• Ultrasound
– Establishes diagnosis easily
– Accurately measures infrarenal diameter
– Difficult to visualize thoracic or suprarenal
aneurysms
– Difficult to establish relationship to renal arteries
– Technician dependent
– Widely available, quick, no risk, cheap

Aortic Aneurysms
CT Scan
• Very reliable and reproducible
• Can image entire aorta
• Can visualize relation ship to visceral vessels
• Longer to obtain and is more costly than U/S
• Most useful
• Requires contrast agent - renal toxicity

Aortic Aneurysms
MRA
 Now widely available
 More expensive than CT
 No contrast agent required
 Spacial resolution less than CT
 Can visualize the whole extent of the aorta in multiple planes
 Ability to assess branch vessels, AI, and pericardial effusion
• In the acute setting, MRI is limited because it is less accessible, it is
• more difficult to monitor unstable patients during imaging, and it
has
• longer acquisition times than CT
 Limited applicability in pts with pacemakers or metallic clips

TEE
 TEE can image the thoracic aorta from the aortic valve to the distal
ascending aorta and from the distal aortic arch to the proximal
abdominal aorta.
 The distal ascending aorta and proximal aortic arch cannot be
reliably imaged by TEE because the intervening trachea and left
mainstem bronchus obstruct the acoustic window; this is known as
the “blind spot” of TEE.
 The advantages of TEE include its portability, its real-time
Interpretation, its compatibility at the bedside and in the OR, and
its multiple imaging modalities for complete aortic and cardiac
assessment.
 Its disadvantages include the requirement for sedation or general
anesthesia and the risks for upper gastrointestinal injury.

Management strategies
Non-surgical management and surveillance
The main aim of medical therapy is to reduce shear stress on the
diseased segment of the aorta by reducing blood pressure and
cardiac contractility
The most important medical management steps are as follows:
(i) Smoking cessation can slow down aneurysmal growth by 15– 20%
and decrease perioperative morbidity relating to wound healing
and cardiorespiratory complications.
(ii) Statins can minimize perioperative myocardial ischaemia
(iii) According to recent recommendations, low-dose aspirin should
be started when an AAA is diagnosed and continued indefinitely may
alter aneurysmal growth
.

• Control of both blood pressure and ejection velocity
are the mainstays of hemodynamic optimization of the
patient with an aortic lesion to prevent aneurysm
rupture.
• Aggressive control of blood pressure with vasodilators
is likely to cause a reflex tachycardia and an increase in
left ventricular change in pressure over change in time
LV (dp/dt), thereby increasing ejection velocity and the
sheer forces on the aortic lesion.
• Simultaneous control of both blood pressure and
ejection velocity is best obtained with a combination of
beta-blockers and vasodilators

• In patients with Marfan syndrome, prophylactic use of
beta-blockers, angiotensin-converting enzyme (ACE)
inhibitor, and angiotensin II receptor blocker seem to
be able to reduce either the progression of the aortic
dilation or the occurrence of complications
• In chronic conditions, blood pressure should be
controlled below 140/90 mm Hg, with lifestyle changes
and use of antihypertensive drugs, if necessary

SCREENING
• Data from the United Kingdom Multicentre Abdominal
Aortic Aneurysm Screening Study (MASS) have shown that
for patients with AAA diameters greater than 55 mm
measured by ultrasonography, the number needed to treat
(NNT) with elective AAA repair to prevent one death from
AAA over the following four years
• The United Kingdom Small Aneurysm Trial showed that
patients with AAA antero-posterior diameters of 40 to 54
mm measured by ultrasonography randomized to elective
surgical treatment were more likely to die from an AAA-
related cause than those randomized to best medical
treatment and screening

RECOMMENDATIONS FOR
INTERVENTION IN AORTIC ANEURYSM

PRE OP EVALUATION
• A preoperative history and examination reveals stridor, wheezing,
cough, or tracheal deviation should raise suspicion of aortic
impingement and possible tracheomalacia.
• Unilateral vocal cord paralysis, which results from compression of
the recurrent laryngeal nerve between the aorta and trachea, may
present clinically as voice hoarseness.
• Preoperative pulmonary function testing with flow–volume loop
analysis will reveal an intrathoracic obstructive process in severe
cases.
• Radiographic studies may be useful in delineating the extent of
airway compromise caused by aortic lesions.

PRE OP AIRWAY ASSESSMENT
• The trachea is markedly
deviated secondary to an
aortic aneurysm.
• The trachea and left
mainstem bronchus may
be compressed from an
aortic aneurysm.
• Left-sided double lumen
endotracheal tubes may
be difficult to place in
these patients

Incidence of coexisting diseases in patients with
aortic pathology presenting for surgery
• Coronary artery disease 66%
• Hypertension 42%
• Chronic obstructive pulmonary disease 23%
• Peripheral vascular disease 22%
• Cerebrovascular disease 14%
• Diabetes mellitus 8%
• Other aneurysms 4%
• Chronic renal disease 3%

Cardiac Assessment
• Because myocardial ischemia is an important predictor of perioperative
outcome, it has featured prominently in the guidelines for thoracic aortic
diseases.
• Patients with evidence of myocardial ischemia should undergo further
evaluation to determine the extent and severity of coronary artery disease
(CAD; ACC/AHA Class I recommendation; level of evidence C).
• If significant CAD is responsible for an acute coronary syndrome, then
coronary revascularization is indicated before or concomitant with the
thoracic aortic procedure (ACC/ AHA Class I recommendation; level of
evidence C).
• Concomitant coronary artery bypass grafting (CABG) is reasonable in
patients who have not only stable but significant CAD, but who are also
scheduled to undergo surgery for diseases of the ascending aorta or aortic
arch, or both (ACC/AHA Class IIa recommendation; level of evidence C

Assessment of organ systems
• 1. Neurologic. patient should be monitored closely for
change in neurologic status, as this is an indication for
immediate surgical intervention. Involvement of the artery
of Adamkewitcz may lead to lower extremity paralysis,
while propagation of a dissection into a cerebral vessel may
lead to a change in mental status or stroke symptoms.
• 2. Renal function. Urine output should be followed, as
development of anuria or oliguria in the euvolemic setting
is an indication for immediate surgical intervention.
• 3. Gastrointestinal. Serial abdominal examinations should
be performed, and blood gas analysis should be done
routinely to assess changes in acid-base status. Ischemic
bowel can cause significant metabolic acidosis

PRE OP MEDICINE
• According to recent recommendations, patients should continue
• taking b-blockers (if already taking these), aspirin, and statins
before surgery.
• Diuretics and ACE inhibitors should be considered on a case-by-
case basis.
• Decisions regarding continuation of clopidogrel and newer
antiplatelet agents ( prasugrel, ticagrelor) through the perioperative
period are more complex and depend on the indication for these
agents;
• Although there is an increased risk of perioperative bleeding,
recent data suggest that continuation of clopidogrel may not
increase transfusion requirements or the incidence of reoperation
for bleeding after AAA repair

Bleeding and transfusion
• Coagulopathy frequently encounterd
• Many pt require Lt heart or full CPB during Sx, CPB may
cause consuptive coagulopathy & enhanced
fybrinolysis, thus ↑ing bl. Loss
• DHCA may cause platelete dysfunction secondary to
extream hypothermia
• So prepare total of 8 to 10 units of PCV, FFP & PC
• Blood scavenging & reprocessing
• Antifibrinolytic therapy during aortic surgery is
controversial but commonly used eg. Trenexamic acid,
ƐACA,Aprotinin

Monitoring
 Minimum standard monitoring should be placed before induction of
anaesthesia.
 A five-lead ECG is more sensitive in detecting myocardial ischaemia.
 Invasive arterial pressure monitoring should be established before but
central venous access is usually secured after induction of anaesthesia.
 Urinary catheterization and temperature monitoring
 Neuromonitoring
 Different cardiac output monitoring strategies have their limitations and
may respond slowly to haemodynamic changes with aortic cross-clamp
application and release.
 Oesophageal Doppler uses flow velocity in the aorta to calculate cardiac
output and is unreliable when the aorta is clamped.
 Pulse wave contour analysis cardiac output and other monitors are gaining
popularity, but their use has not yet been fully evaluated in aortic surgery

ARTERIAL CANNULATION
• A right radial arterial catheter is preferred for most cases.
• If arterial cannulation of the right axillary, subclavian, or
innominate artery is planned for CPB and ACP, bilateral radial
arterial catheters often are required to measure cerebral and
systemic perfusion pressures
• Asc. Aortic lesion may involve the Innominate A., so Lt Radial or
femoral line is inserted for direct BP monitoring.
• If Rt. Axillary cannulation is used arterial pr measurement will be
falsely elevated bec. Of increased flow.
• In case of Descending aortic and thoracoabdominal aneurysms
(TAA) Arterial monitoring lines are inserted in the right radial and
femoral arteries to monitor proximal and distal pressures during the
period of aortic cross-clamping. The femoral line is valuable when
left-heart bypass techniques are used

Induction
 Anaesthesia is no different from that for conventional open heart sx
 The induction of general anesthesia requires careful hemodynamic monitoring
with anticipation of changes because of anesthetic drugs and tracheal intubation.
• Appropriate vasoactive drugs should be immediately available as required.
• Avoid hypertension to increases forward flow in AR and minimizes the risk for
aneurysm rupture.
 Concomitant vasodilator infusions often are discontinued before anesthetic
induction.
 Because etomidate does not attenuate sympathetic responses with no direct
effects on myocardial contractility, it may be preferred in the setting of
hemodynamic instability.
 In elective cases, anesthetic induction can proceed with routine intravenous
hypnotics, followed by narcotic titration for attenuation of the hypertensive
responses to tracheal intubation and skin incision.
 General anesthetic maintenance is typically with a balanced technique with
narcotic and inhalation agent , neuromuscular blockade is achieved by titration of
a nondepolarizing muscle relaxant

Surgical repair in different type of
aortic aneurysm
• The type of surgical repair depends on aortic valve function
and the aneurysm extent.
• The most common aortic valve diseases associated with
ascending aortic aneurysm are bicuspid aortic valve or AR
caused by dilation of the aortic root.
• If the aortic valve and aortic root are normal, a simple tube
graft can be used to replace the ascending aorta.
• If the aortic valve is diseased but the sinuses of Valsalva are
normal, an aortic valve replacement combined with a tube
graft for the ascending aorta without need for
reimplantation of the coronary arteries can be performed;
ACC/AHA class I recommendation; level of evidence C).

• If disease also involves the aortic valve and the aortic
root, the patient requires aortic root replacement and
aortic valve intervention.
• If technically feasible, the aortic valve can be
reimplanted with a modified David technique, which
includes graft reconstruction of the aortic root with
reimplantation of the coronary arteries (ACC/AHA Class
I recommendation; level of evidence C).
• If not feasible, aortic root replacement with a
composite valve-graft conduit is indicated (Bentall
procedure ACC/AHA Class I recommendation; level of
evidence C).

Surgery in aortic arch aneurysm
• For ascending aortic aneurysms that involve only the proximal aortic arch,
partial arch replacement (hemiarch technique) is reasonable in which a
tubular graft is interposed between the ascending aorta or aortic root and
the underside of the aortic arch (ACC/AHA Class IIa recommendation;
• Ascending aorta with hemiarch reconstruction often is performed using
DHCA with or without ACP/RCP to make the distal anastomosis feasible
without cross-clamping (“open technique”).
• In patients who have isolated aortic arch aneurysms and who have a low
operative risk, arch replacement is reasonable when the arch diameter
exceeds 5.5 cm (ACC/AHA Class IIa recommendation;
• Total aortic arch replacement is reasonable in aneurysms that involve the
entire arch (ACC/AHA Class IIa recommendation
• Ascending aortic aneurysms that extend through the aortic arch into the
descending aorta can be repaired with the “elephant trunk” technique
ACC/AHA Class IIa recommendation;

CANNULATION FOR CPB
 If the aneurysm ends in the proximal or midportion of the ascending aorta, the arterial cannula for
CPB can be placed in the upper ascending aorta or proximal arch.
 Femoral artery cannulation is particularly useful in emergency situations with hemodynamically
unstable pa tients. However, it creates retrograde flow in the abdominal and thoracic aorta, it is a
potential cause of embolic stroke in patients with heavy atherosclerotic burden
 Most recommeded and newer approach is to cannulate the right axillary , or occasionally the right
carotid, artery, allowing perfusion into the innominate artery and then into the aorta in an
antegrade manner
 Most commonly venous drainage by right atrial dual-stage cannula, bicaval cannulae, .
 Femoral venous cannulation is routinely used in hemodynamically unstable patients who require
pump support before sternotomy and is particularly useful in patients who are at risk of aortic
injury during sternotomy. In patients undergoing reoperation and large ascending aortic aneurysms
abutting the sternum

• During systemic cooling in aortic aneurysm surgery the heart will spontaneously
fibrillate. At this time, a left ventricular VENT is inserted through the right superior
pulmonary vein to decompress the left ventricle. This is especially important in
patients who are prone to ventricular distention, such as those with aortic valve
regurgitation.
• To prevent this complication, the Vent is generally placed before systemic cooling
begins.
• If the patient has an incompetent aortic valve, as may be the case in an aortic
dissection, manual compression of the distending heart may be necessary at this
time
• Other advantage of LV vent are to
 Minimizes preload,
 Prevents ventricular distention,
 Reduces myocardial rewarming,
 Prevents ejection of air,
 Facilitates exposure of the aortic valve.

MYOCARDIAL PROTECTION
• Cardioplegia is achieved with the use of a cold hyperkalemic
crystalloid or blood cardioplegic solution, which may be administered
in one of several ways:
(a) antegrade aortic root administration if the aorta can be cross-
clamped and the aortic valve is competent,
(b) direct coronary ostial administration after opening of the
ascending aorta, or
(c) retrograde administration through the coronary sinus.
• When the aortic arch is included in the procedure and when cross-
clamping of the ascending aorta is not possible because of excessive
friability of the aortic tissues, DHCA is required.

TEE
• Perioperative TEE can evaluate the aortic valve
structure and function to guide and assess the surgical
intervention (reimplantation,repair, replacement).
• Furthermore, TEE can assess the diameters of the
aortic root, ascending aorta, and aortic arch to guide
intervention..
• In patients with AR, TEE can assist in the conduct of
CPB by guiding placement of cannulae such as the
retrograde cardioplegia cannula (coronary sinus) and
by monitoring left ventricular (LV) volume to ensure
that the LV drainage cannula keeps the ventricle
collapsed.

Brain Protection for Aortic
Arch Reconstruction
• Deep systemic hypothermia
• • Topical cerebral cooling
• • Retrograde cerebral perfusion
• • Selective antegrade cerebral perfusion
• • Cerebral hyperthermia prevention during
rewarming

DEEP HYPOTHERMIA AND
CIRCULATORY ARREST
• Deep hypothermia is the mainstay of any operation that
requires opening the distal ascending aorta or transverse
aortic arch where blood flow to the brain must be
interrupted.
• Although there may be controversy about the best
method of cerebral perfusion during surgeries that
involve the aortic arch, deep hypothermia alone will
usually provide the surgeon with a safe arrest period of
30 minutes, provided the patient's brain is cooled to
<20°C.

Conduct of DHCA
• The cooling phase should be gradual and long enough(20-30 mins) to
achieve homogenous allocation of blood to various organs and to prevent
a gradual updrift of temperature during DHCA
• The most effective method of cooling for DHCA is core cooling on high-
flow CPB.
• Cooling temperatures never exceeding 10° C differences between the
perfusate temperature (circuit) and the patient core temperature.
• Perfusate temperature is maintained between 10° C and 15° C during
cooling.
• A vasodilator such as sodium nitroprusside or phentolamine (0.2 mg/kg)
may be administered into the CPB circuit as core cooling commences to
promote vasodilation and more homogenous cooling

Organ protection during DHCA
• Hypothermia
• Pharmacological adjuncts
• Perfusion strategies
• Topical external cooling of the head
• optimized acid-base management
• pump prime modifications
• leukocyte depletion
• The degree of hemodilution
• strategies of cooling and rewarming

α-stat vs pH-stat
• pH-stat strategy results in greater cerebral blood flow, greater
efficiency, and uniformity of brain cooling, and higher brain
oxyhemoblobin saturation and less reduced cytochrome a,a3
signifying more oxygen at the mitochondrial level than α-stat blood
gas management
• However, other data suggest that cerebral metabolic recovery after
DHCA may be better with the α-stat method than with the pH-stat
mode
• Some institute use crossover strategy in which a pH-stat approach is
used during the first 10 minutes of cooling to provide maximal
cerebral metabolic suppression, followed by an α-stat strategy to
remove the severe acidosis that accumulates during profound
hypothermia during pH-stat

Rewarming strategies
 There is no more than 10° C temperature differential
between the core and perfusate temperatures.
 Patients should warm at the same rate at which they
were cooled.
 Warming rate should never exceed 1° C core
temperature increase per 3 minutes of bypass time.
 Use of vasodilators to facilitate distal perfusion
 Treat metabolic acidosis agressive
 Termination of warming should occur when the
nasopharyngeal temperature is between 35° C and 36°
C. This mild hypothermia provides additional cerebral
protection in the early postoperative period.

Pharmacologic Neuroprotection
 There are no proven pharmacologic regimens that have demonstrated
effectiveness for decreasing the risk or severity of neurologic injury in the
setting of thoracic aortic operations.
 The agents that have been reported in aortic arch series include
thiopental, propofol, steroids, magnesium sulfate, and lidocaine
 Furthermore, there is considerable variation in practice with these agents
in aortic arch repair
 The technique of DHCA with pharmacologic adjuncts is a reasonable
approach for neuroprotection during aortic arch surgery in the setting of
an institutional protocol and adequate institutional experience (ACC/AHA
Class IIa recommendation; level

Retrograde cerebral perfusion
• RCP is performed by infusing cold oxygenated blood
into the superior vena cava cannula at a temperature
of 8° C to 14° C via CPB
• The internal jugular venous pressure is maintained at
less than 25 mm Hg to prevent cerebral edema
• Patient is positioned in 10 degrees of Trendelenburg
to Decrease the risk for cerebral air embolism and
prevent trapping of air
• Flow rates of 200 to 600 mL/min usually can be
achieved

• Advantage are more homogeneous cerebral cooling;
washout of air bubbles, embolic debris, and metabolic
waste products; prevention of cerebral blood cell
microaggregation; and delivery of oxygen and
nutritional substrates to brain tissue
• During RCP, only a minimal amount of blood (not more
than 3% to 10%) is directed to the brain, whereas more
than 90% is deviated through the azygos to the SVC or
entrapped in the cerebral venous sinuses

Anterograde cerebral perfusion
• Arterial CPB circuit flow can be delivered selectively to the
cerebral circulation antegrade via the circle of Willis following
cannulation of the innominate artery or right carotid artery
• ACP may be unilateral or bilateral, there remains controversy about
which ACP technique is superior. A recent literature Showed the
period of safe ACP was significantly prolonged with bilateral ACP
compared with unilateral ACP (30–50 minutes). The evidence favors
bilateral ACP in the setting of aortic arch repair times longer than 60
minutes
• The technique of DHCA with ACP is a reasonable approach for
neuroprotection during aortic arch surgery in the setting of
adequate institutional experience (ACC/AHA Class IIa
recommendation; level of evidence B).

GOALS OF Anaesthetic management
IN TAAA OPEN REPAIR
• Anaesthetic management focuses on the
Acute haemodynamic changes with aortic
cross-clamping and unclamping,
Maintaining organ perfusion and oxygenation
Attenuating ischaemic reperfusion injury,
 Providing intra- and postoperative analgesia

Lung Isolation Techniques
• Selective ventilation of the right lung with
concomitant left lung Collapse during TAAA repair
enhances surgical access and protects the right
lung from left lung bleeding.
• Collapse of the left lung typically is achieved
when the left main bronchus is intubated either
with a double-lumen endobronchial tube (DLT) or
a bronchial blocker.
• The advantages of a left DLT include the ability to
apply selective continuous positive airway
pressure to the left lung

analgesia
 A thoracic epidural catheter is usually placed before
induction of anaesthesia at a level corresponding to
the upper dermatomal level of the incision (usually T8–
T10) for Postoperative analgesia
 Intraoperative analgesia can be provided using opioids
or by using epidural analgesia;
 however, high doses of epidural local anaesthetics can
cause profound hypotension after aortic crossclamp
release due to sympathetic blockade.
 It is common practice to limit epidural local
anaesthetic administration until after crossclamp
release and haemostastis has been achieved.

 Heparin 75–150 units kg21 is given i.v. before aortic
crossclamp application.
 Activated clotting time can be used to guide heparin
therapy (2–3 times more than baseline).
 Cell salvage equipment should be used when available.
 Serial arterial blood gas samples are usually analysed
to monitor respiratory and metabolic status.
 Facilities for the rapid infusion of warm fluids and
blood should be available for immediate use.
 All efforts should be made to maintain normothermia;
however, lower body warming during aortic cross-
clamp application is discouraged

RECOMMENDATION FOR PERFUSION
TECHNIQUE
 Descending thoracic aortic repairs
Left heart bypass for high-risk patients (acute dissection, rupture,
prior abdominal aortic aneurysm repair)
 Extent I and II thoracoabdominal repairs
Left heart bypass during proximal anastomosis
Selective perfusion of celiac axis and superior mesenteric artery
during intercostal and visceral anastomoses
Perfusion of renal arteries with 4°C crystalloid solution
 Extent III and IV thoracoabdominal repairs
Perfusion of renal arteries with 4°C crystalloid solution

Open repair of TAAA typically is accomplished
by one of three major PERFUSION techniques;
(1) aortic cross-clamping,
(2) aortic cross- clamping with a Gott shunt,
(3) aortic cross-clamping with PLHB or partial
CPB

Simple Aortic Cross-Clamp Technique
• Its major Disadvantage is the concomitant vital organ
ischemia below the aortic clamp.
• Its further disadvantages include proximal aortic
hypertension, Bleeding, and hemodynamic instability
on reperfusion.
• Proximal aortic hypertension may induce LV Ischemia.
• Mild systemic hypothermia and selective spinal cooling
protect against the ischemia associated with this
technique.
• Despite its physiologic consequences, this technique
remains popular because it is simple and has proven
clinical outcomes

Gott Shunt
 The Gott shunt allows passive
shunting of blood from the proximal
to distal aorta during aortic cross-
clamping for thoracic aortic repair
 Blood flow from the proximal to
distal aorta through the Gott shunt
depends on proximal aortic
pressure, shunt length and diameter,
and distal aortic pressure.
 Monitoring the femoral arterial
pressure facilitates assessment of
distal aortic perfusion and shunt
flow.
 The advantages of the Gott shunt
are its simplicity, its low cost, and its
requirement for only partial
anticoagulation.

Partial Left-Heart Bypass
• The control of both proximal and
distal aortic perfusion during TAAA
repair is achieved with PLHB.
• This technique requires left atrial
cannulation, usually via a left
pulmonary vein
• Oxygenated blood from the left
atrium flows through the CPB circuit
into the distal aorta or a major
branch via the arterial Cannula.
• The degree of heparinization for
PLHB is minimal with heparin-coated
circuits without an oxygenator.
• Full systemic anticoagulation with
ACT greater than 400 seconds is
required for CPB circuits with
membrane oxygenators and heat
exchangers

• During PLHB, the proximal mean arterial pressure (MAP; radial artery) is
generally maintained in the 80 to 90 mm Hg range.
• Flow rates in the range of 1.5 to 2.5 L/min typically maintain a distal aortic
MAP in the 60 to 70 mm Hg range, monitored via a femoral arterial
catheter.
• Sequential advancement of the aortic crossclamp during PLHB permits
segmental aortic reconstruction with a decrease in end-organ ischemia.
• The advantages of PLHB include control of aortic pressures and systemic
temperature, reliable distal aortic perfusion, and selective antegrade
perfusion of important branch vessels

Advantages of distal perfusion
• Control of proximal hypertension
• Decrease left ventricular afterload
• Less hemodynamic perturbations with aortic clamping and
unclamping
• Decrease duration of mesenteric ischemia
• Decrease risk for paraplegia from spinal cord ischemia
• Ability to control systemic temperature with heat exchanger
• Vascular access for rapid volume expansion
• Ability to oxygenate blood with extracorporeal oxygenator
• Capability to selectively perfuse mesenteric organs or aortic branch
vessels
• Maintain lower extremity SSEPs and MEPs for neurophysiologic
monitoring

aortic cross-clamping
 The physiological effect of aortic cross-clamping during
surgery varies with the level of the clamp in relation to
the main aortic branches.
 Perfusion to the lower half of the body is therefore
dependent on collateral circulation while the clamp is
applied.
 Clamp application increases the afterload of the heart
and a sudden increase in arterial pressure proximal to
the clamp; this can be ttenuated with vasodilators [e.g.
glyceryl trinitrate (GTN), sodium nitroprusside],
opioids, or deepening of anaesthesia.

• Increased afterload and left ventricular end-
diastolic volume both increase myocardial
contractility and oxygen demand.
• This increase in myocardial oxygen demand is
usually met by an increase in coronary blood flow
and oxygen supply, but can cause myocardial
ischaemia
• The mean arterial pressure should be maintained
within the autoregulation limits of vital organs.

aortic cross-clamp release
After aortic cross-clamp release, peripheral vascular resistance
decreases by 70–80%, causing a decrease in arterial pressure.
Hypotension can also be caused by blood sequestration in the
lower half of the body, ischaemia–reperfusion injury, and the
washout of anaerobic metabolites causing metabolic (lactic) acidosis.
This can cause direct myocardial suppression and profound
peripheral vasodilatation. Coronary blood flow and left ventricular
end-diastolic volume also decrease (almost 50% from pre-clamp
levels) after clamp release

MANAGEMENT OF AORTIC
CROSSCLAMP RELEASE
• Strategies to manage hypotension after aortic cross-clamp release include
 Discontinue vasodilator agents
 Gradual release of the clamp,
 Volume loading,
 Vasoconstrictors, or
 Positive inotropic drugs (e.g. ephedrine, termine phenylephrine,
epinephrine, and norepinephrine).
• It is important to be aware that vasoactive drugs should only be used after
adequate volume repletion
• TEE can adequately assist with LV volume assessment.
• Acidosis may be treated with hyperventilation and bolus administration of
sodium bicarbonate.
• A continuous infusion of bicarbonate (0.05 mEq/kg/min) during cross-
clamping may be more efficacious.

RENAL PROTECTION
• The main cause of renal complications after AAA repair is the
decrease in renal blood flow, decreased renal perfusion pressure
(outside autoregulation) augmented by the increasing renal
vascular resistance (by 30%) associated with aortic clamping.
• Myoglobin release from ischaemic tissues may contribute to acute
tubular necrosis by decreasing local nitric oxide release.
• Acute kidney injury (AKI) may also be linked to ischaemic– perfusion
injury, decreased renal cortical blood flow, prostaglandin imbalance,
and increased activity of renin–angiotensin system.
• Postoperative dialysis rates are similar in patients who have
undergone either suprarenal or infra-renal aortic cross-clamping

• Rhabdomyolysis from lower extremity ischemia was recently
identified as a mechanism for renal dysfunction after TAAA repair.
• The maintenance of lower extremity perfusion bilaterally during
distal aortic perfusion has been shown to ameliorate this
rhabdomyolysis with a significant nephroprotective effect
• intraoperative cold renal perfusion with blood or crystalloid is
recommended as a reasonable intraoperative nephroprotective
strategy during TAAA repair (ACC/AHA Class IIb recommendation;
level of evidence C).

• The thoracic aortic guidelines recommend preoperative
hydration and intraoperative mannitol administration as
reasonable nephroprotective strategies in extensive distal
open thoracic aortic repairs, including TAAA repair
(ACC/AHA Class Iib recommendation; level of evidence C).
• Several drugs (dopamine, N-acetyl cysteine, mannitol,
furosemide) have been used in an attempt to protect
against AKI, although none has been shown consistently to
be beneficial, and all diuretics should be used only after
adequate fluid replacement and volume loading.
• Mannitol can increase renal blood flow during aortic cross-
clamp; however, both mannitol and dopamine use fail to
return GFR to baseline levels after operation

PARAPLEGIA IN TAAA REPAIR
• Paraplegia after TAAA repair is a
devastating complication.
• most patients, one radicular arterial
branch, known as the great radicular
artery (of Adamkiewicz), provides a
major portion of the blood supply to
the midportion of the spinal cord. It
may arise anywhere from T5 to below
L1
• The temporary interruption of distal
aortic perfusion and sacrifice of
spinal segmental arteries during
TAAA repair are central events in the
pathogenesis of spinal cord ischemia
and paraplegia
•

Factors That Contribute to Paraplegia after Thoracic
or Thoracoabdominal Aneurysm repair
 Duration of aortic cross-clamp
 Thoracoabdominal aortic
aneurysm extent
 Hypotension or cardiogenic shock
 Emergency surgery
 Aortic rupture
 Presence of aortic dissection
 Sacrifice of intercostal or
segmental artery branches
 Prior thoracic or abdominal aortic
aneurysm repair
 Occlusive peripheral vascular
disease
 Anemia

Techniques to Decrease the Risk
for Intraoperative Spinal Cord Ischemia
 Distal aortic perfusion
 Arterial pressure augmentation
 Minimizing the ischemic time
 Mild systemic hypothermia
 Lumbar cerebrospinal fluid drainage
 Selective spinal cord cooling
 Segmental aortic reconstruction
 Intercostal artery preservation
 Pharmacologic neuroprotection
 Intraoperative motor- or somatosensory-evoked potential
monitoring

Minimize Aortic Cross-clamp Time
 Distal aortic perfusion
• Passive shunt (Gott)
• Partial left heart bypass
• Partial cardiopulmonary bypass
 Deliberate Hypothermia
• Mild-to-moderate systemic hypothermia (32° C to 35°
C)
• Deep hypothermic circulatory arrest (14° C to 18° C)
• Selective spinal cord hypothermia (epidural cooling,
25˚ C)

Increase Spinal Cord Perfusion
Pressure
• Reimplantation of critical intercostal and
segmental arterial branches
• Lumbar cerebrospinal fluid (CSF) drainage (CSF
pressure ≤ 10 mm Hg)
• Arterial pressure augmentation (mean arterial
pressure ≥ 85 mm Hg)

spinal drain management
• SCPP is estimated as the MAP minus the lumbar CSF
pressure.
• In general, the SCPP should be maintained greater than 70
mm Hg
• 30% or more of all neurologic deficits are delayed in onset
• spinal drains are commonly left in for 48 hours
postoperatively and are replaced if neurologic deficits occur
after the drain is removed.
• maintain CSFP between 10 to 15 mm Hg in the
postoperative setting, efforts must be made to avoid
systemic hypotension and associated decreased spinal cord
perfusion.
•

Intraoperative Neurophysiologic
Monitoring
• Neurophysiologic monitoring of the spinal cord (SSEPs
and/or MEPs) is recommended as a strategy for the
diagnosis of spinal cord ischemia so as to allow immediate
intraoperative neuroprotective interventions such as
intercostal artery implantation, relative arterial
hypertension, and CSF drainage (ACC/AHA Class IIb
recommendation; level of evidence B).
• Because SSEP monitors posterior spinal column integrity,
MEPs have been advocated because they monitor the
anterior spinal columns that are most common at risk
during TAAA repair.

Spinal Cord Hypothermia
 Although DHCA is effective, moderate systemic hypothermia is also
reasonable for spinal cord protection during TAAA repair (ACC/AHA
Class IIa recommendation; level of evidence B).
 Furthermore, topical spinal cord hypothermia is possible with cold
saline epidural infusion to avoid ischemia during TAAA repair.
 Epidural cooling is recommended as an adjunctive technique for
spinal cord protection during major distal thoracic aortic
reconstructions (ACC/AHA Class IIb recommendation; level of
evidence B).
 This technique give adjunctive benefit and the recent clinical
development of a specialized countercurrent closed-lumen epidural
catheter for epidural cooling during major distal aortic
reconstructions

Pharmacologic Protection of the Spinal
Cord
• Pharmacologic spinal cord protection with agents
such as high dose systemic glucocorticoids,
mannitol, intrathecal papaverine, and anesthetic
agents is recommended as an adjunctive
technique in a multimodal neuroprotective
protocol (ACC/AHA Class IIb recommendation;
level of evidence B).
• Additional neuroprotective agents that have
been studied in this regard include lidocaine,
naloxone, and magnesium

TEVAR
• Thoracic endovascular aortic repair aims at
excluding an aortic lesion (i.e. aneurysm or FL
after AD) from the circulation by the
Implantationof a membrane-covered stent-
graft across the lesion, in order to prevent
further enlargement and ultimate aortic
rupture

TEVAR Anesthetic Protocol
• Always GA for TEVAR
• For EVAR General Anesthesia ,Regional Anesthesia
(epidural alone or spinal or combined) or Local Anesth
(local groin infiltration) with sedation
• Assess risk of SCI
• Consider spinal drain
• Neuromonitoring
• Arterial line The right radial artery is preferred for
• blood pressure monitoring, given that the left subclav
artery frequently may be covered and/or the left brac
artery may be accessed as part of the procedure.
• PAC monitoring may be helpful in the setting of signif

GA VS REGIONAL OR LOCAL
• Risk‐adapted Outcome after Endovascular Aortic
Aneurysm Repair: Analysis of Anesthesia Types Based
on EUROSTAR data
• Ruppert et al. Journal of Endovascular Therapy, 2007.
• between 1997 and 2004, 164 centers, 5557 patients
• Patients were divided into low‐risk (ASA I or II.), high
risk(ASA III or IV), LA, GA, RA into 6 groups.
• Low‐risk group: 78.8% GA, 15.9% had RA, 5.3% LA
• High‐risk group: 60.4 % GA, 33.7% RA, 5.9% LA

• Outcomes
• • GA vs. RA or LA:
• less systemic complications
(cardiac, cerebral,
pulmonary, renal,
• hepatobiliary, sepsis)
• • GA versus RA: less 30 days
early death in the RA group
• • Less ICU admission with
local and regional (low risk
and high risk )

• Observation from the IMPROVE trial (BJS 2014)
• Prospective multicenter, observational study on
Anesthesia type in 558 patients with a
symptomatic or ruptured aneurysm ( EVAR )
• Lowest blood pressure (<70 MAP) was strongly
and independently associated with 30‐days
mortality
• • EVAR with local anesthesia (adjusted to
variables) alone had greatly reduced (4 fold) 30
days mortality

pre-procedural planning
• Contrast-enhanced CT
represents the imaging
modality of choice for
planning TEVAR, taking ,3
mm ‘slices’ of the proximal
supra-aortic branches down
to the femoral arteries
RECOMMENDATION FOR TEVAR

TEE IN TEVAR
• Intraoperative TEE is reasonable in thoracic
aortic procedures, including endovascular
interventions, in which it assists in
hemodynamic monitoring, procedural
guidance, and endoleak detection (ACC/AHA
Class IIa recommendation; level of evidence

Complications
• Immediate conversion to open surgery is required in
approximately 0.6% of patients.
• .
• The rates of vascular injury after EVAR are low
(approximately 0–3%), due to careful pre-procedural
planning.
• The incidence of stent-graft infection after EVAR is ,1%,
with high mortality.
• Graft migration
• Embolisation

Classification of
endoleaks.
Endoleak is the most
common complication of
EVAR.
Type I and Type III
endoleaks demand
correction (proximal cuff
or extension),
Type II endoleak may
seal spontaneously in
about 50% of cases

spinal cord
ischemia after TEVAR or EVAR
• perioperative hypotension (decreased SCPP),
• prior abdominal/descending thoracic aortic
procedures (compromised spinal collateral
arterial network)
• coverage of the entire descending thoracic
aorta (significant loss of intercostal arteries

Spinal cord protection protocol
• Place CSF drain the pre procedure
• Record opening pressure, zero at RA level
• If pressure exceeds 12 mmHg, pressure goal < 10mmHg
• Limit CSF drain to less than 20 ml over 1st‐hr
• Limit CSF drain to less than 40 ml over 4‐hours
• If SSEP signal decrease drain 10 ml
• MAP > 90 hgmm post‐TEVAR
• Clamp drain after confirming bilateral lower extremity
function
• Remove drain after 24 hrs of clamping
• Reopen/Drain if delayed paraparesis/paraplegia
• If CSF turns bloody turn off drain

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