09 hashem et al

© Acta Anæsthesiologica Belgica, 2007, 58, n° 1
Abstract : Thoracoabdominal aortic aneurysms are one
of the most challenging surgeries for the anaesthetists.
They account for 10% of aneurysms of the aorta. A
thorough understanding of pathophysiology, anatomy,
and surgical interventions including extracorporeal cir-
culation are essential to achieve a good outcome.
Crawford classified them accorting to their their extent
and location in 4 types. Patients with Crawford type II
aneurysms are at greatest risk for paraplegia and renal
failure from ischemia to the spinal cord and kidneys
during cross-clamp. Neurologic and renal complications
are significant for the most extensive forms of
aneurysms. Mortality has improved over time as a conse-
quence of either increased surgical experience, the adop-
tion of a protocolized strategy for repair, or secular
improvements in anaesthetic and intensive care treat-
ment. Long-term survival after elective TAAA repair is
excellent.
INTRODUCTION
Thoracoabdominal aortic aneurysms (TAAA)
are one of the most challenging type of intervention
for the anaesthesiologist. These aneurysms are
defined as aneurysms involving either the thoracic
and abdominal aorta or the suprarenal segments of
the abdominal aorta (1). A thorough understanding
of pathophysiology, anatomy, and surgical interven-
tions including extracorporeal circulation are essen-
tial to achieve a good outcome.
PREVALENCE
TAAA account for 10% of aneurysms of the
aorta, and aortic aneurysms are present in 1-4% of
the population over 50 years of age. Greater
longevity, improved detection, better community
awareness of this disease are likely to lead to
increasing numbers of patients undergoing surgery
for TAAA repair (2).
AETIOLOGY AND CLASSIFICATION
A true aortic aneurysm is a dilation of the
entire aorta, as measured across from the adventitia
to the adventitia, and it is associated with degener-
ative changes of the aortic wall where the original
histological constituents can still be recognized.
Only one half of TAAA are atherosclerotic in ori-
gin. The remainder are caused either by trauma or
by connective tissue diseases involving the aortic
wall from conditions such as Marfan syndrome,
cystic medial degeneration, Takayasu arteritis, or
syphilitic aortitis. Patients with aneurysmal disease
have a poor prognosis without surgery. Nutritional
blood flow to the aorta is compromised, and the
increasing diameter is associated with increased
wall tension (LaPlace’s law), even when arterial
pressure is constant (2). In view of the often lethal
consequence of ruptured aneurysms, for men age
65 to 75 years, an invitation to attend screening
reduces aneurysms-related mortality (15).
Crawford classified TAAA in type I, II, III,
and IV according to the anatomic extent (Table 1
and Fig. 1) (3). This classification has been further
revised by Dr Cinà to include a broader range of
anatomical situations found in clinical practice.
Surgeons dealing with this condition, in fact, may
have to replace the entire aorta from the aortic valve
to the bifurcation (type VI) or varying segments of
the thoracic and abdominal aorta which do not nec-
essarily fall within Crawford’s classification
(Fig. 2). Patients with Crawford type II aneurysms
(Acta Anaesth. Belg., 2007, 58, 45-54)
Anaesthesia for surgical repair of thoracoabdominal aortic
aneurysms
M. HASHEM (*) and C. S. CINÀ (**)
M. HASHEM, M.D., FFARCSI ; C. S. CINÀ, M.D., FRCSC, MSc
(HRM)
(*) Senior Specialist Registrar, Singleton Hospital, Swansea,
UK. mahashem63@hotmail.com
(**) Division of Vascular Surgery, Department of Clinical
Epidemiology and Biostatistics, McMaster University,
Hamilton, Ontario, Canada.
Corresponding address : Dr. C. S. Cinà, 304 Victoria Ave.
N. # 305, Hamilton, Ontario, L8L 5G4, Canada.
E-mail : cinacs@mcmaster.ca.

46 M. HASHEM AND C. S. CINÀ
are at greatest risk for paraplegia and renal failure
from ischemia to the spinal cord and kidneys during
cross-clamp. Even with extra-corporeal circulatory
support, there is an obligatory period of time when
blood flow to these organs is interrupted. For this
reason, protective measures to prevent ischemic
injury are important in reducing morbidity.
PRE-OPERATIVE CO-MORBIDITIES AND EVALUATION
Patients with thoracoabdominal aortic
aneurysms often have multiple comorbidities which
affect not only life expectancy but also periopera-
tive outcome (Table 2) (4). Because of the impor-
tance of preoperative cardiac, pulmonary and renal
status on morbidity and mortality the importance of
a thorough preoperative assessment of these sys-
tems should be emphasised (Table 3). In addition,
the preoperative nutritional status is important and
needs to be carefully evaluated and, if necessary,
improved. Low preoperative serum albumin level
has been associated with postoperative negative
outcomes in surgical patients. For this reason it is
our practice to evaluate in all patients’ albumin and
total serum proteins. In those with low albumin or
with clinical evidence of malnutrition, our practice
is to supplement their diet with a high protein/
calorie beverage (e.g., ensure 2 cans per day) during
the month before surgery.
Table 1
Crawford’s Classification of Thoracoabdominal Aneurysms
Group Location and Extent of Aneurysm Description
Type I Involves the descending thoracic aorta from the left subclavian artery to the celiac
artery, just below the diaphragm.
Mostly thoracic aorta
Type II Includes aneurysms involving most of the descending thoracic and most of the
abdominal aorta, from the left subclavian artery to the bifurcation of the aorta.
Most of thoracic and abdominal aorta
Type III
Involves the lower portion of the thoracic aorta and most of the abdominal aorta.
Lower thoracic aorta and abdominal aorta
Type IV Most of the abdominal aorta up to and including the celiac artery, just above the
diaphragm.
Mostly abdominal aorta
Fig. 1. — Crawford’s Classification of Thoracoabdominal
Aneurysms.
Fig. 2. — Cina’s proposed classification of aneurysmal disease
of the entire thoracoabdominal aorta.

Airway and chest
The chest x-ray should be available in the
operating room and should be examined preopera-
tively for evidence of aneurysm compression of the
left main stem bronchus (5). Preoperative pul-
monary assessments provide a baseline measure-
ment to aid in risk stratification, and to identify
patients whose preoperative respiratory status may
be improved. Poor pulmonary function is associat-
ed with prolonged respiratory ventilation and
increased mortality. All patients should have
spirometry, arterial blood gas and analysis study of
gas diffusion. The lower limit for FEV1 below
which significant activity restriction and carbon
dioxide retention occurs is around 0.6 to 0.7 L. In
patients with carbon dioxide retention, the five year
survival is less than 10%. In patients undergoing
abdominal aneurysm surgery the transient postoper-
ative decrease in FEV1 is at least 0.6 L. Because of
the extensive involvement of the abdomen and tho-
rax, the division of the diaphragm and other physi-
ological derangements in TAAA surgery, the
decrease in FEV1 will be greater. Svenson suggests
an FEV1 of below 1.2 L, a carbon dioxide level of
greater than 45 mm Hg, an FEV 25% of less than
0.5 L/sec, and a PaO2 of less than 55 mm Hg as pre-
operative indicators of high risk for postoperative
respiratory complications (6).
Cardiac assessment
The extent of the cardiac investigation is con-
troversial. It is prudent, however, to have an exten-
sive cardiac work-up in these patients since most
patients should be assumed to have cardiac disease.
We prefer to investigate all patients with coronary
angiography. We feel that the results of the CARP
trial are not applicable to this patient population
since patients with thoracoabdominal aortic
aneurysms were not included in this study (21).
However, an alternative strategy may be to use two-
dimensional echocardiography, exercise stress test
or Persantin Thallium investigation and Holter elec-
trocardiography (for the detection of silent
ischemia, and atrial or ventricular arrhythmias) to
try to risk stratify these patients. Those patients
with coronary artery disease are considered for pre-
operative revascularization (either with percuta-
neous transluminal dilatation and stenting or with
coronary artery bypass graft) before surgery or
occasionally, inpatients operated on an emergency
basis, during surgery (combined off-pump bypass
on beating heart and TAAA repair). Beta-blocker
therapy usually starts preoperatively unless such
therapy is contraindicated. Several authors and
guidelines committees have advocated the use of
b-blockers in patients having non-cardiac surgery.
The robustness of the evidence for this intervention
has been questioned. Perioperative b-blockers may
decrease the risk of major perioperative cardiovas-
cular events but increase the risk of bradycardia and
hypotension needing treatment. The beneficial
results, however, are based on only a moderate
number of major events, and the findings depend on
methodologically weak trials. Methods adapted
from formal interim monitoring boundaries applied
to cumulative meta-analysis show that the evidence
for perioperative b-blockers is insufficient and
inconclusive (13).
THORACOABDOMINAL AORTIC ANEURYSMS 47
Table 2
Comorbidities in patients with TAAA
1- Hypertension, 70%
2- Coronary artery disease, 35%
3- COPD, 35%
4- Visceral occlusive disease 25%
5- Chronic renal failure, 20%
6- Cerebrovascular disease, 15%
7- Peripheral vascular disease, 15%
8- Diabetes mellitus, 5%
Table 3
Care map : preoperative phase
1- Optimisation of lung function – Abstinence from smoking for at least 1 month
– Bronchodilators, inhaled steroids, and antibiotics
2- Prophylaxis of cardiac complications – Therapy with beta or calcium channel blockers and ACE inhibitors
– Interventional therapy (PTCA, CABG)
3- Optimisation of renal function – Hydration
– Pretreatment with N-acetylcisteine
4- Optimisation of haemostasis – INR, PTT, platelet
– Preparation of an adequate amount of blood product anticipating 5-6 L of blood losses

Blood Losses and Blood Products Utilization
Repair of TAAA is associated with major
blood losses, often exceeding the patient’s intravas-
cular volume, and complex intraoperative and post-
operative coagulopathies necessitating large-vol-
ume transfusion of blood products. Abnormalities
sufficient to cause thrombocytopenia or clinically
important prolongation of clotting parameters are
rarely present before surgery in elective aneurysms
but are more common with ruptured aneurysms.
The coagulation abnormality identified before sur-
gery is that of higher PTT values, suggesting a dis-
turbance of the extrinsic coagulation pathway (1).
The finding of intraoperative and postoperative
deficiencies of clotting factors, along with thrombin
generation and activation of the thrombolytic sys-
tem, is reflective of massive blood losses, visceral
ischemia, and massive transfusions. An aggressive
strategy of transfusion of blood products is critical
to the prevention of clinically significant coagu-
lopathy during surgery. Adjuncts to reduce blood
losses and blood product use include low-dose
aprotinin, tranexanic or epsilon -aminocaproic acid,
intraoperative blood salvaging, and acute normov-
olemic hemodilution. In TAAA repair, an average
blood loss of 5000 to 6000 mL and average transfu-
sion of allogeneic blood products of 50 to 60 units
are to be anticipated (16). Blood and clotting fac-
tors should be available. We recommend an initial
cross match 12-16 units of packed red blood cells,
10 units of fresh frozen plasma and 10 units
platelets (5).
Renal function
A preoperative serum creatinine concentration
of greater than 200 mmol/L has been associated
with a 42% incidence of postoperative renal failure
defined by creatinine greater than 265 mmol/ or the
need for dialysis, following TAAA repair. Renal
failure is also associated with a higher incidence of
respiratory failure and postoperative paraplegia.
Acetylcysteine used as an adjunct during TAAA
was associated with a trend to improved renal func-
tion (18).
Peripheral vascular disease
Manifestations of peripheral vascular disease
need to be identified. If there is evidence of carotid
artery stenosis surgical correction may be indicated
prior to surgery. In addition attention to femoral and
radial pulses is important since multiple arterial
lines for upper and lower body systemic blood pres-
sure are often necessary for monitoring during sur-
gery (2). In addition if an atrio-femoral by pass is
used, disease of the aorto-iliac-femoral system may
require special surgical considerations that need to
be carefully discussed with the surgeon.
ANAESTHETIC MANAGEMENT
Table 4 summarizes the challenges associated
with providing anaesthesia for patients undergoing
TAAA repair. In order to reduce complications and
mortality, multiple surgical and anaesthetic tech-
niques such as different adjuncts for distal aortic
perfusion (DAP), cerebrospinal fluid drainage, and
regional cooling of the spinal cord and kidneys have
been developed. These techniques are controversial
and not universally accepted because complications
such as renal failure and paraplegia still occur (2).
A care plan should be drawn for the intraoperative
phase (Table 5).
Monitoring and Infusion Lines
If partial bypass is not used, the primary focus
should be on massive blood loss and the ability to
rapidly transfuse. It is preferred to place at least
three large bore intravenous lines for transfusion.
The right jugular vein is avoided to prevent the pos-
sibility of pneumothorax in a patient who will be on
the right lateral decubitus and single right lung ven-
tilation. A Swan-Ganz catheter is also routinely
inserted (5). In cases when partial bypass is used,
the primary focus is often the coordination of upper
body blood flow and lower body blood flow. The
perfusionists usually maintain a mean distal arterial
pressure of 60 to 70 mmHg. Since the left atrium is
supplying the left ventricle (for upper body perfu-
sion) and the bypass circuit (for lower body perfu-
sion), it is apparent that if the perfusionists increase
Table 4
Perioperative problems of TAAA (2, 4)
1- Higher risk patients, ASA III-IV elderly patients
2- One lung ventilation (OLV)
3- Profound haemodynamic changes caused by clamping and
unclamping of the thoracic aorta
4- Massive blood losses
5- Coagulopathy
6- Severe metabolic derangement
7- Vital organs ischemia or damage e.g. renal and spinal cord
9- Prolonged post operative course
10- Expensive operation

the pump flow enough, it will eventually compro-
mise left ventricular filling, which immediately
compromises proximal pressure and perfusion (e.g.
brain and heart). The use of electromagnetic pump
which is volume-controlled (as opposed to a rotary
pump) minimizes the risks of this complication.
Maintenance of adequate intravascular volume and
communication between anaesthetists and the per-
fusionists are essential. We prefer to use three arte-
rial lines, one in each radial (the left radial may be
lost if the clamp is placed proximal to the left sub-
clavian artery), and one in the right femoral artery
to monitor proximal and distal pressures (5).
The use of transoesophageal echocardiogra-
phy is helpful (7). Chronic diastolic dysfunction
(DD) is a well-recognized problem in hypertensive
patients and in patients with high afterload present-
ing for TAAA. The relationship between left ven-
tricular diastolic relaxation and systolic function
may be uncoupled. As a result, many of the tradi-
tional monitors of cardiac systolic function may not
reflect the extent of diastolic dysfunction.
Transesophageal echocardiography (TEE) is neces-
sary to measure the alterations in intracardiac flows
and velocities to assess the extent of DD . Filling of
the Left Ventricle occurs in diastole in two different
phases. The first phase, known as E-wave, starts
with mitral valve opening, and blood flow occurs
during the relaxation of the LV. The second, known
as A-wave, occurs at the end of diastole as a conse-
quence of atrial contraction. The majority of filling
of the LV occurs during the E-wave (> 85%).
Echocardiographically, with normal diastolic func-
tion the velocity of blood during the E-wave is
therefore greater than during the A-wave. In condi-
tions of diastolic dysfunction, atrial contraction
contributes relatively more to ventricular filling,
and the blood velocity during A wave becomes
greater than in the E wave causing an inversion of
the E : A ratio. In TAAA repair, there is a sudden
increase in afterload during aortic clamping. The
reversal of E : A ratio identified by TEE during aor-
tic clamping in TAAA repair was reported (19).
Other uses of TEE in TAAA repair include visual-
izing the position of left atrial (LA) cannula when
left atrio-femoral bypass (LAFB) is used and to
monitor the LV function and volume (19). Beta-
blockers may be protective of intra-operative acute
diastolic dysfunction (13).
Airway Management
Patients operated on an emergency basis will
be considered to have a full stomach. In these situ-
ations the benefits of a rapid sequence (airway pro-
tection) must be balanced against the patient’s
haemodynamic status (5). We often use bronchial
blockers for one lung anaesthesia. They are easier
to place than double lumen tubes. However, it takes
a longer time for the lung to deflate and they do not
allow for separate lung ventilation. A disadvantage
of double lumen tubes is that at the end of the case
they need to be changed to a single lumen endotra-
cheal tube at a time when airway and facial oedema
are present, or they must be left in place until the
oedema is resolved with consequence caused by
pressure due to their stiffness and increase airway
resistance. The position of the bronchial blocker
should be checked (and rechecked in the lateral
position) with the fiberoptic bronchoscope.
The Pre-Clamp Period
Blood pressure should be well controlled to
prevent rupture, to allow easier management of the
post-clamping hypertension, and to reduce blood
losses. Before the aortic cross clamp is applied,
mannitol at approximately 0.5-1.0 g/kg is usually
Table 5
Care map ; Intraoperative Phase
1- One lung anaesthesia • Double lumen tube or endobronchial blocker.
• Confirmation of position with patient supine and in lateral decubitus
2- Transfusion therapy – ANH
• Anticipatory treatment of coagulation disorders (FFP, Cryoprecipitate, inhibitors of fibrinolysis)
3- Antimicrobial therapy • Cefazolin 2 g before induction of anaesthesia and 1g after loss of 1 blood volume
4- Prevention of renal dysfunction • Cold perfusion (blood, or crystalloid)
• Target parenchymal temperature < 20 ϱC
• Low dose dopamine, frusemide, mannitol.
• N-acetylcysteine
5- Prevention of paraplegia • CSF drainage
• Target pressure < 10 cm H2O
• Reattachment of intercostals arteries from T7-L1

administered because of its diuretic and free oxygen
radicals scavenger properties which may be benefi-
cial for renal and spinal cord protection. If partial
bypass is used (atrial or pulmonary vein to femoral
artery) there is usually partial heparinization
(100 I.U./kg). If full bypass is used (femoral-
femoral with an oxygenator) full heparinization is
used to maintain an activated clotting time of 400 to
450 seconds (6). The senior author described the
use of acute normovolaemic haemodilution with
partial exchange transfusion (ANHPET) in surgery
of TAAA. During TAAA repair, ANHPET was used
to withdraw of up to 3 L of blood. This was returned
to the patient at the end of the reconstruction.
Albumin 5% and stored packed red cells (PRC)
were used for replacement. ANHPET reduced
blood product transfusion, improved postoperative
haemostatic parameters and simplified the manage-
ment of cross-clamping hypertension (1, 7). This
appears to be a useful adjunct in the anaesthetic
management of TAAA patients.
Preparation for Aortic Cross Clamping Without
Bypass
Nitroprusside, labetalol, esmolol and or intra-
venous nitroglycerine should be available for
immediate infusion as needed to control blood pres-
sure. However, arterial blood pressure should be
maintained at a mean of 70 to 90 mmHg after the
clamp is applied. This is because perfusion distal to
the clamp (spinal cord, kidney, etc.) is severely
diminished and the use of vasodilators further exac-
erbates low end-organ perfusion. The needs of the
heart (which would prefer a lower afterload) need to
be balanced against those of the poorly perfused
end-organs. Once the aneurysm is opened, there
may be substantial blood loss. A cell-saver and
rapid infusion systems should be used with large
bore intravascular access for rapid transfusions.
Platelets and fresh frozen should be given to avoid
complex forms of dilution and consumption coagu-
lopathies (16). Calcium chloride should also be
given, either guided by ionized calcium levels or
one gram for every three units of packed cells (6).
Preparation for removal of the Aortic Cross Clamp
without Bypass
Additional platelets and fresh frozen, and cry-
oprecipitate are often given just before aortic
unclamping to prevent bleeding secondary to coag-
ulopathy and to provide increase preload. If a con-
tinuous infusion of bicarbonate was not adminis-
tered during clamping (usually 0.005 mmoL/Kg/
minute), 100 mmoL of bicarbonate are slowly
administered at this point to balance reperfusion
acidosis. One additional gram of calcium may be
also given at this point. An infusion of low dose
(0.005-0.01 ug/kg/min.) norepinephrine is often
started approximately 5-10 minutes before the aor-
tic cross clamp is removed. At this point it is often
advisable to have another anaesthetist to help in this
critical phase. All blood products should be in the
room and checked. Normally with cross clamp
removal there is reactive hyperaemia, vasodilata-
tion, and decreased systemic vascular resistences
and preload. The surgeon should remove the cross
clamp slowly to prevent profound hypotension and
the clamp may be reapplied, if necessary until the
volume status and haemodynamic drugs are opti-
mized (6).
Preparation for Aortic Cross Clamping With
Bypass
Partial bypass is initiated before cross clamp-
ing ; minimal effect on blood pressure is seen with
cross claming. The proximal cross clamp is then
applied slowly, and distal flows are titrated to main-
tain adequate proximal and distal pressures. If prox-
imal pressure falls it is usually because there is
inadequate volume to support the flow rates that the
perfusionists are trying to achieve. Flow rates must
temporarily be decreased, and slowly reestablished.
Typically, distal pressures can be about 50 to
60 mmHg, while proximal pressures should be
equal or slightly below preclamp pressures (5). We
use a modified circuit which consists of a primary
circuit with a centrifugal pump and heat exchanger
to perfuse and warm the systemic circulation and a
parallel secondary circuit with a roller pump and a
second heat exchanger to perfuse the viscera with
cold blood. A progressive sequential cross-clamp-
ing technique is used. This technique offers theoret-
ical hemodynamic and metabolic advantages and
may prove to be useful in preventing ischemic and
reperfusion injury to the spinal cord and kid-
neys (8).
Preparation for Removal of the Aortic Cross Clamp
with Bypass
With perfusion to the lower body with partial
or full bypass, acidosis and hypovolemia are often
less troublesome compared with clamp and go tech-
nique. The perfusionists gradually reduce the flow
rates allowing proximal pressure to rise and the

clamp is gradually released. Volume or pressors
may be needed initially, so blood should be in the
room and checked (usually the haematocrit is kept
at 25-30% throughout the case and have at least
2 units of PRBC pressurized and ready to infuse at
cross clamp removal). However, as the surgeons are
assessing their repair it is important to avoid hyper-
tension (5).
Renal Protection
Lasix, mannitol or dopamine may be used in
an attempt to preserve renal function. Any of these
adjuncts are able to augment flow through the renal
tubules, however, there is little scientific basis on
which to choose one or a combination of them. We
know, however, that hypovolemia or decreased
cardiac output increases the likelihood of renal fail-
ure (20). Patients at increased risk include those
with pre-existing renal compromise, older patients,
longer cross clamp times (greater than 30 minutes),
and failure to use atrial-femoral bypass. Acute renal
failure occurs in 3-14% with a mortality rate
approaching 40% (4). Many renal protective agents
have been used, including acetylcysteine with some
encouraging results (18).
Spinal Cord Protection
Paraplegia may result from prolonged
ischemia (long cross clamp times, particularly those
above 30-45 minutes) or the occlusion of the artery
of ADAMKIEWICZ (4). Aortic occlusion increases
cerebrospinal fluid pressure (CSFP), which increas-
es after aortic cross clamp (likely caused by
increased venous congestion of dural veins) and
decreases distal aortic systolic pressure, thereby
decreasing perfusion of the spinal cord. Theoreti-
cally, decreasing CSFP by cerebrospinal fluid
drain-age (CSFD) should improve spinal cord
blood flow and decrease the risk of spinal cord
ischemic injury. One approach is to place a lumbar
epidural catheter into the subarachnoid space to
drain CSF. This is done before the procedure
begins. The hope is that draining CSF will lower the
CSF pressure and allow more blood flow, since
spinal cord perfusion pressure (SCPP) is equal to
mean arterial pressure (MAP) minus cerebral spinal
fluid pressure (CSFP). Dropping the CSF pressure
to 10cm H20 might double blood flow by doubling
the gradient of pressure. If catheters are placed,
they should not be removed until it is been docu-
mented that coagulation status has returned to nor-
mal. Usually 20-40 cc drained before cross clamp-
ing, then either they can passively drain, or about
10 cc/hr of CSF can be removed, throughout the
case (4). Evidence from randomized and non ran-
domized trials and from cohort studies support the
use of CSF drainage as an adjunct to prevent
paraplegia when this adjunct is used in centres
with large experience in the management of
TAAA (17).
Some centres use electrophysiologic monitor-
ing with somatosensory evoked potentials (SSEP)
and motor evoked potentials (MEP) to monitor for
spinal cord ischemia (2). However there are some
problems associated with SSEP monitoring
(Table 8). These monitoring techniques may be
helpful in identifying the important intercostal
arteries that perfuse the spinal cord so they can be
implanted into the graft. If ischemia is identified,
cross-clamps can often be moved, upper or lower
body blood pressure can be increased to provide
perfusion through collaterals. Other measures may
include CSF drainage, induced hypothermia, or
intrathecal papaverine (2).
Table 6
Difference between full CPB machine and LVAD machine
Full CPB machine LVAD device
Oxygenator Yes No
Reservoir Yes No (patients acts as a reservoir)
Heat exchanger Incorporated with oxygenator Separate (no oxygenator)
Management of HTN Decrease flow Proximal HTN ; Increase flow
Distal HTN ; decrease flow
Management of Hypotension Increase flow Proximal HTN ; decrease flow if no response ± vasopresors
(guided by filling pressures)
Distal HTN ; increase flow
Priming volume 1800 ml 600 ml
Heparin (for 70 kg patient) 280 mg (28000 IU) 5000 IU

Stimulation over the motor cortex or the cervi-
cal spine with sensing over the popliteal nerve is the
most commonly used technique. Body temperature
should be monitored at two sites (core and periph-
eral) to assess cooling and warming on bypass.
There is an important difference, however, between
full and partial bypass with regard to temperature
monitoring : with full bypass, perfusion is usually
into the ascending aorta, and typically the upper
body core temperature (nasopharynx or oesopha-
gus) cools and warms fastest, whereas the lower
body temperature changes more slowly ; with par-
tial bypass, the opposite occurs. The blood from
bypass is returned into the femoral artery, and the
lower body (rectum or bladder) changes before the
upper body changes. This difference is important to
recognize in order to achieve complete cooling and
warming because the lagging temperature should be
the end point for cooling and warming.
LATE OPERATIVE AND POSTOPERATIVE CONSIDERATIONS
By the end of the procedure, patients could be
hypovolemic, oedematous, very cold with marginal
lung function. So very often patients are ventilated
overnight while kept in a 30 degree head up posi-
tion so that head oedema can resolve before extuba-
tion or change in the tracheal tube. A care plan
should be drawn for the postoperative (Table 7).
Table 7
Care map : Postoperative phase
1- PEEP of 10 mmHg in the first 12 h
2- Maintain normo- or moderate hypervolemia
3- Aggressive treatment of coagulation disorders
4- CSF drainage for 48-72 h
5- Close surveillance of infections
6- Liberal use of broad spectrum or multiple antibiotics
7- Early use of AVF or dialysis
8- Early use of TPN
Table 8
Problems with SSEP monitoring (2)
1- Poor monitor for the anterior columns. As a result, paraplegia can
occur in spite of normal SSEP signals.
2- Inhaled anaesthetics and hypothermia can interfere with SSEP
signals.
3- Ischemia affects peripheral nerves, and ischemia to the lower
extremities delays conduction from the usual stimulation sites (poste-
rior tibial nerve).
Table 9
Evaluation of Competing Factors for Death for TAAA
1- Cardiac – A symptomatic patients ; 2D- ECHO and Cardiac Nuclear Studies
– Symptomatic patients ; Coronary angiography
• Negative, for TAAA
• Positive, PTCA or CABG before TAAA
2- Pulmonary PFTs plus ABGs
3- Renal ; calculate GFR Cockroft-Gault formula = (140- Age) ϫ Body weight in Kg (lean)/Cr (ϫ 0.85 -for female only)
• Life Expectancy Manulife ; Life Expectancy calculator
Fig. 3. — Venous cannula through the upper pulmonary vein,
connected to the left ventricle assistance device (LVAD), left
atrium (LA) (9).

MORBIDITY AND MORTALITY
Trials should be made preoperatively to evalu-
ate competing factors for death for TAAA (Table 9).
In a series of 121 patients, Cina reported an overall
hospital mortality of 21.4% : 12% for the elective
and 64% for the ruptured group, respectively. The
overall incidence of neurologic deficits due to
spinal cord ischaemia was 6.2% (paraplegia in
4.4%). Age, sex, diabetes mellitus, Detsky index,
presence of dissection, use of LVAD (Table 6,
Fig. 3), CSF drainage, and volume of CSF fluid
drained were not associated with the presence or
absence of neurologic dysfunction. Temporary dial-
ysis was necessary in 13% of patients, and chronic
in 2%. In long-term follow up of patients undergo-
ing elective repair five-year survival was 80%, and
median survival was 7.9 y (9). This was in contrary
to Roilier, who reported the incidence of paraplegia
in patients undergoing surgical repair of TAA to be
from 5 to 40 percent, depending on the anatomic
location, the duration of cross- clamp, the use of
protective measures, the degree of dissection, and
whether the aneurysm has ruptured (11).
Renal failure was reported to occur in 3 to
30% of patients depending on similar factors.
Svensson reported that 6 percent of patients needed
postoperative dialysis after TAA repair, which is
associated with high mortality (30-60%) (11).
Factors associated with hospital mortality are illus-
trated (Table 10).
CONCLUSION
Mortality has improved over time as a conse-
quence of either increased surgical experience, the
adoption of a protocolized strategy for repair, or
secular improvements in anaesthetic and ITU care.
Neurologic and renal complications are significant
for the most extensive forms of aneurysms. Long-
term survival after elective TAAA repair is excel-
lent.
References
1. Cina C., Clase C. M., Bruin G., A cohort study of coagula-
tion parameters and the use of blood products in surgery of
the thoracic and thoracoabdominal aorta, J. VASC. SURG.,
33 (3), 462-8, 2001 Mar.
2. Norris E., Anesthesia for vascular surgery. In : Miller’s
Anesthesia, sixth edition, Elsevier Churchill Livingstone,
Philadelphia, Pennsylvania, p 2081-2089, 2005.
3. Crawford E. S., Thoracoabdominal and supra-renal
abdominal aortic aneurysm. In : Emst C. B., Stanley I. C.,
eds. Current Therapy in Vascular Surgery. Philadelphia,
Decker, p 96, 1987.
4. Robe J., Carell T., Neidhart P., Anaesthetic management of
patients undergoing surgery on descending aorta,
BAILLIERE’S CLINICAL ANAESTHESIOLOGY, volume 14, No 1,
pp 173-186, 2000.
5. Alessi R., Ellis J., Descending Thoracic (Thoracoabdomi-
nal) Aortic Aneurysm, Vascular Thoracic Anesthesia
Manual, University Of Chicago, Internet resource, July 24,
1996.
6. Svensson L. G., Crawford E. S., Hess K. R., et al.,
Experience with 1509 patients undergoing thoracoabdom-
inal aortic operations, J. VASC. SURG., 17, 357-370, 1993.
7. Cina C., Clase C. M., Bruin G., Effects of acute normo-
volaemic haemodilution and partial exchange transfusion
on blood product utilization, haemostasis and haemody-
namics in surgery of the thoracoabdominal aorta. A cohort
study in consecutive patients, PANMINERVA MED., 42 (3),
211-5, 2000 Sep.
8. Cina C. S., Irvine K. P., Jones D. K., A modified technique
of atriofemoral bypass for visceral and distal aortic perfu-
sion in thoracoabdominal aortic surgery, ANN. VASC.
SURG., 13 (6) : 560-5, 1999 Nov.
9. Fayad A., Sawchuk, Yang H., Cina C., Transesophageal
echocardiography in the management of left atrio-femoral
bypass during thoracoabdominal aortic aneurysm repair :
a case report, CAN. J. ANAESTH., 49 (10) : 1081-3, 2002
Dec.
10. Cina C., Lagana A., Bruin G., Ricci C., Doobay B.,
Tittley J., Clase C. M., Thoracoabdominal aortic aneurysm
repair : a prospective cohort study of 121 cases, ANN. VASC.
SURG., 16 (5) : 631-8, 2002 Sep. Epub 2002 Aug 19.
11. Roilier L. R., Money S. R., Naslund T. C., et al., Risk of
spinal cord dysfunction in patients undergoing thoraco-
abdominal aortic replacement, AM. J. SURG., 164, 210,
1992.
12. Svensson L. G., Coselli I. C., Safi H. I., et al., Appraisal of
adjuncts to prevent acute renal failure after surgery on the
thoracic or thoracoabdominal aorta replacement, J. VASC.
SURG., 10, 230, 1989.
13. Devereaux P., Beattie W., Choi P., Badner N., Guyatt G.,
Villar J., Cinà C., Leslie K., Jack M., Montori V.,
Bhandari M., Avezum A., Cavalcanti A., Giles J.,
Schricker T.,Yang H., Jakobsen C.,Yusuf S., How strong is
Table 10
Factors associated with hospital mortality (10)
Factor Statistical significance
1- Age ; 67 y in survivors vs. 73 y in non survivors P = .03
2- FEV1 less than 2 L RR 4.1, P = 0.01.
3- CSF drainage RR 5.0, P = 0.03.
4- Type II aneurysms vs. other aneurysms RR 3.7, P = 0.02.
5- Relative inexperience Mean rank in series was 52 in survivors vs. 30 in non survivors, P = 0.01.

the evidence for the use of perioperative b-blockers in non-
cardiac surgery ? Systematic review and meta-analysis of
randomised controlled trials, BMJ, 6, 331 (7512), 2005
August.
14. McFalls E., Ward H., Moritz T., Goldman S., Krupski W.,
Littooy F., Pierpont G., Santilli S., Rapp J., Hattler B.,
Shunk K., Jaenicke C., Thottapurathu L., Ellis N., Reda D.,
Henderson W., Coronary-Artery Revascularization before
Elective Major Vascular Surgery, N. ENGL. J. MED., 30,
351 (27), 2795-804, 2004 Dec.
15. Fleming C., Whitlock E., Beil T., Lederle F., Screening for
abdominal aortic aneurysm : a best-evidence systematic
review for the U.S. Preventive Services Task Force, ANN.
INTERN. MED., 1, 142 (3), 203-11, 2005 Feb.
16. Cina C., Clase C., Coagulation disorders and blood prod-
uct use in patients undergoing thoracoabdominal aortic
aneurysm repair, TRANSFUS. MED. REV., 19 (2), 143-54,
2005 Apr.
17. Cinà C., Abouzahr L., Arena G., Laganà A., Devereaux P.,
Farrokhyar F., Cerebrospinal fluid drainage to prevent
paraplegia during thoracic and thoracoabdominal aortic
aneurysm surgery : a systematic review and meta-analysis,
J. VASC. SURG., 40 (1), 36-44, 2004 Jul.
18. Cina C., Jhirad R., Laganà A., Hashem M., Clase C.,
Acetylcysteine : an adjunct for renal protection in thoraco-
abdominal aneurysm repair, GAZZETTA MEDICA ITALIANA,
163 (6), 233-8, 2004 Dec.
19. Fayad A., Sawchuk C., Yang H., Cina C., Transesophageal
echocardiography in the management of left atrio-femoral
bypass during thoracoabdominal aortic aneurysm repair :
a case report, CAN. J. ANAESTH., 49 (10), 1081-3, 2002 Dec.
20. Mehta R., Pascual M., Soroko S., Chertow G. for the
PICARD Study Group, Diuretics, Mortality, and
Nonrecovery of Renal Function in Acute Renal Failure,
JAMA, 288, 2547-2553, 2002.
21. McFalls E., Ward H., Moritz T., Goldman S., Krupski W.,
Littooy F., Pierpont, Santilli S., Rapp J., Hattler B.,
Shunk K., Jaenicke C., Thottapurathu L., Ellis N., Reda D.,
Henderson W., Coronary-Artery Revascularization before
Elective Major Vascular Surgery, N. ENGL. J. MED., 351,
2795-2804, 2004 Dec.

09 hashem et al

Recommended

Recommended

More Related Content

What's hot

What's hot (20)

Viewers also liked

Viewers also liked (12)

Similar to 09 hashem et al

Similar to 09 hashem et al (20)

Recently uploaded

Recently uploaded (20)

09 hashem et al