Anaesthesia for abdominal aorta

aneurysm repair

Presenter : Dr. Richa Malik

Moderator : Dr. Ajay Kumar
 Contents
Introduction
Preoperative evaluation & optimisation in vascular surgery
Abdominal aortic aneurysm : definition, classification
Etiology
Epidemiology
Clinical features & natural history
Open repair vs EVAR
Anaesthesia for open AAA repair
Anaesthesia for EVAR
Postoperative complications
 Introduction
The perioperative management of patients undergoing vascular surgery is one of the
most challenging and controversial areas in the field of anesthesiology
Given the frequent occurrence of coexisting disease in elderly patients , the
hemodynamic and metabolic stress associated with arterial cross-clamping and
unclamping, and the ischemic insults to vital organs, including the brain, heart, kidneys,
and spinal cord, peri-operative morbidity and mortality are more frequent with vascular
surgery than with most other surgical procedures
 Preoperative evaluation
Patients undergoing vascular surgery have a frequent incidence of coexisting disease,
including
•

• Diabetes mellitus
• Hypertension
• Renal impairment
• Pulmonary disease
• Coronary artery disease
All of which should be assessed and, if possible -optimised prior to sx
 ROLE OF PREOPERATIVE
EVALUATION
Not to give medical clearance
To perform an evaluation of the patient’s current medical status
Make recommendations concerning the evaluation, management, & risk for cardiac
problems
Provide a clinical risk profile that the patient & caregivers can use in making treatment
decisions that may influence perioperative & longer term cardiac outcomes
The overriding theme of the perioperative guidelines is that preoperative testing should
not be performed unless it is likely to influence patient care.
 Preanesthetic evaluation
Cardiac function : baseline ECG, additional cardiac testing only in patients with
change in symptoms & functional status

Pulmonary function : h/o smoking, COPD, ABG, PFT

Renal function : S. Creatinine - elevated preoperatively is the strongest predictor of

post renal dysfunction post open aortic surgery & is also a predictor of CV
complications & mortality

Preop Lab tests : CBC, Coagulation fxn tests, electrolytes, glucose

Typing & crossmatching for blood and blood products

 Preoperative medications
Cardiovascular medications : Statins, beta blockers, aspirin should be continued
throughout the perioperative period

Statins :
1

1 lipid-lowering, anti-inflammatory, plaque stabilising, antioxidant properties

2 Statin use can help preserve renal function after aortic surgery and improve
graft patency after lower extremity bypass surgery

OHA :
 Abdominal aortic aneurysm
An aneurysm is typically defined as a greater than 50% dilation of the expected
normal arterial diameter

The aorta tapers gradually from the thorax to the abdomen such that its normal diameter
at the level of the renal arteries is approximately 2.0 cm

FACTORS such as age, gender, race, and body surface area may influence normal aortic
diameter, an abdominal aortic diameter greater than 3.0 cm is considered
aneurysmal

Aortic aneurysm occurs most commonly in the abdominal aorta

Aneurysms of the thoracic and thoracoabdominal aortas occur far less commonly
 Classification
Abdominal aortic aneurysms (AAAs) are classified by location as

Infrarenal (originating below the level of the renal arteries),

Juxtarenal (originating at the level of the renal arteries),

Suprarenal (originating above the renal arteries)

This distinction is important because it dictates the complexity of the surgical repair
and the potential for hemodynamic derangements, particularly with open
intervention and the accompanying aortic cross-clamp

The majority of AAAs are infrarenal, whereas approximately 5–15% involve the
suprarenal aorta.
Crawford classification of
thoracoabdominalDefinedaortic
by
• anatomic location
the extent of involvement.
and

aneurysms Type I aneurysms involve all or

•

most of the descending thoracic

aorta and the upper abdominal
aorta;
• Type II aneurysms involve all or
most of the descending thoracic
aorta and all or most of the
abdominal aorta;
• Type III aneurysms involve the
lower portion of the descending
thoracic aorta and most of the
abdominal aorta;
 Etiology
Degenerative : most common etiology

Inflammatory

Infective

Trauma

Congenital conditions

connective tissue disorders

 Etiology
Process of aneurysm formation is a distinct degenerative progression with features such
as vessel wall infiltration by macrophages, destruction of elastin and collagen, loss of
smooth muscle cells, and neovascularization

While inflammation and macrophage infiltration are common to both atherosclerotic

and aneurysmal disease, atherosclerosis is primarily noted within the intima and
media, whereas aneurysmal disease typically affects the media and adventitia
 Epidemiology of AAA
AAAs are typically seen in older adults with an incidence that increases significantly
after age 50

The occurrence of AAA is also more common in men and Caucasians

Prevalence : 5%, &t his is decreasing, perhaps as a result of better risk factor
modification

Nonmodifiable risk factors for AAA : age, gender, and family history

Modifiable risk factors : smoking, obesity, hyperlipidemia, hypertension, &

atherosclerotic arteriopathy (including CAD)
 Epidemiology of AAA

Smoking is the modifiable risk factor most strongly associated with AAA

Regular exercise and a healthy diet : decreased risk

In contrast to most vascular pathophysiology, diabetes mellitus is associated with a

reduced risk of AAA

Protective effect of diabetes against AAA may be the consequent vascular stiffness
and calcification, preventing aneurysm formation
 Clinical features
Most AAAs are asymptomatic and are often discovered incidentally

Occasionally, patients may present for vague abdominal pain and/or may note a pulsatile
abdominal mass

Rarely, a large AAA may be secondary to a mass effect on related structures, such as
vomiting from gastrointestinal compression, urinary symptoms from ureteral
compression, or venous complications from iliocaval compression

Most aneurysms eventually become symptomatic secondary to growth or rupture.

 Clinical features
Rupture of an AAA is most often lethal with a mortality rate of at least 75%.

In this setting, of the 50% of patients who reach the hospital alive, about 50% will
survive to hospital discharge

Given these high mortality rates from rupture and emergency surgery in patients with
AAAs, a major management goal is to identify and treat AAAs before they rupture
 Role of Screening

Current European and North American guidelines recommend ultrasound screening for
AAAs in high-risk circumstances, such as for adults older than 64 years and adults with
a family history of AAA 1

Furthermore, the frequency of surveillance imaging for patients with known AAA is a
function of aneurysm size
 Indications for Abdominal Aortic
• The singleAneurysm Intervention
greatest risk factor for aneurysm rupture is size.
• Current evidence-based guidelines suggest repair when aneurysm diameter
exceeds 5.0–5.5 cm.
• Rapid aneurysm growth, defined as greater than 10 mm per year, is also an
indication for intervention.
• Furthermore, urgent repair is recommended in the setting of symptomatic
nonruptured AAA, regardless of size.
• Finally, in the setting of excessive perioperative risk, medical rather than
surgical management may be considered in patients with multiple significant
 Open repair V/S EVAR
• Two strategies - open AAA repair and EVAR
• The decision for open versus endovascular repair for the individual patient depends
on multiple factors, such as aortic anatomy, urgency, patient preference, and surgical
expertise
• Open repair in young patients
• EVAR in older patients with significant coexisting morbidities
 Evidence for open repair V/S
EVAR
EVAR provides a short-term survival benefit but no long-term survival benefit

No difference in either cardiac or aneurysm-related mortality between groups at either

intermediate- or long-term follow-up

Significantly higher rate of reintervention in the endovascular group, although the

majority of these reinterventions were endovascular-based procedures associated with a
low mortality rate
 Additional factors influencing
surgical decision
In the current era, open repair of AAA : reserved for patients who are not candidates for
EVAR

Anatomic constraints posing the greatest barrier to EVAR: A hostile proximal aortic
neck ;compromise adequate endovascular seal because of factors such as short length,
excessive angulation, heavy calcification, or high thrombus burden.
 Additional factors influencing
surgical decision
Challenging iliac artery anatomy such as calcification, aneurysm, and/ or stenosis :
problem for both adequacy of distal endovascular seal and safety of arterial access

Involvement of the abdominal visceral aortic segment is not necessarily a

contraindication to EVAR because current techniques allow for branched, fenestrated,
or snorkeled grafts to maintain patency of visceral vessels such as the renal arteries
 Additional factors influencing
surgical decision
Infection of either the native aorta or aortic graft calls for open intervention

Patients with unique vascular anatomy, such as anomalous renal arteries or in whom the
inferior mesenteric artery is paramount for intesti- nal perfusion, may be better served
with open repair

Complications related to previous EVAR (such as endoleak or migration) that are not
amenable to further endovascular intervention require open repair
 Contraindications for EVAR
ABSOLUTE
Aortic neck diamater > 32 mm at the renal
arteries: problem with adequate proximal seal
Ruptured AAA with aortic neck length < 7mm: at
least 15 mm of undilated aorta below the renal
arteries is ideal to achieve an adequate seal
between endograft & aortic neck
RELATIVE
More than 40% of the aortic neck diameter
occupied with thrombus
Circumferential calcification at aortic neck
Aortic neck angulation > 60 degrees
Bilateral iliac arteries < 6.5cm in diameter
 Conversion from EVAR to Open
repair
Bleeding can’t be controlled with end-vascular balloon occlusion

The graft cannot be positioned or deployed

Large endoleaks or continued bleeding are evident after graft deployment

Anaesthesia for open repair
 Induction
General anaesthesia + Epidural analgesia

Surgical exposure is obtained by either a midline transabdominal or lateral

retroperitoneal incision.

Given the extensive incision and frequency of COPD, epidural analgesia facilitate high-
quality pain control, limit the side effects of parenteral narcotics, and preserve
respiratory function

TEA catheter insertion in the immediate preop , prior to induction of GA

 Induction
Goal : maintain patient’s baseline hemodynamics in order to maintain adequate end-
organ perfusion (typically within 20% of baseline values), while minimizing
sympathetic stimulation to noxious events such as endotracheal intubation and
placement of invasive monitors

Etomidate/low dose propofol + opioid in moderate dose/ lidocaine to blunt

sympathomimetic response to laryngoscopy & intubation
 Induction & Maintenance
In patients susceptible to developing hypotension { old age, intravascular volume
depleted, diastolic dysfunction }, aesthetic drugs to be given slowly, titrated.

Patients developing marked hypertension due to laryngoscopy& intubation - risk of

rupture - Esmolol to treat hypertension & tachycardia

Maintenance : inhalation agents / intravenous- inhalational anesthetics have a

cardioprotective effect, not demonstrated in vascular surgery

Nitrous oxide : avoided d/t bowel distension & increased PONV risk
 Monitoring during anesthesia
Standard monitoring : ecg, spo2, NIBP

Continous ECG monitoring with leads II & V5, with computerised ST segment
trending to detect myocardial ischemia, arrhythmia : more sensitive & superior

Invasive arterial pressure monitoring :

•

• arterial line ideally placed prior to induction

• D/t associated peripheral arterial atherosclerosis, discrepancies in BP btw right &
left upper extremities
•
 Monitoring during anesthesia
• Central venous catheter : to provide large bore venous access, for vasoactive drug
infusions
• PAC : in settings of severe RV dysfunction or pulmonary hypertension
• CVP, PAWP : poor predictor of intravascular volume status, fluid responsiveness
• TEE : To monitor cardiac function & intravascular volume status because of the high
risk of hemodynamic instability & adverse perioperative cardiovascular events,
particularly during aortic cross clamping & unclamping
 Role of TEE
Avoid hypovolemia or hypervolemia

Detection of global or regional ventricular dysfunction, new RWMA : early recognition

of myocardial ischemia or ventricular dysfxn faciltates management

Assessment of cause of hypotension : either due to decreased preload due to

venodilation or myocardial dysfxn secondary to metabolic acidosis

Detection of aortic pathology such as atheroma, thromboembolism or air embolism or

aortic dissection resulting from cannulation or cross clamping of aorta
 Role of point of care testing

• ABG, Electrolytes, blood glucose, hemoglobin, ACT

• ROTEM/ TEG : IN C/O EXCESSIVE BLEEDING or evidence of coagulopathy
• 3 sets of measurements important : baseline, during aotic clamping and after
unclamping prior to extubation
 Temperature management
• Core and peripheral temperature monitoring : any time gradient > 2 degrees indicative
of low cardiac output
• Warming devices to maintain normothermia
• Upper & lower body forced air warming devices & blankets
• Warm I/v fluids
• Lower body forced air warmer should be turned off during the period of aortic cross
clamping because organs distal to the clamp may be hypoperfused and become
ischemic
• Avoid hypothermia and shivering : coagulopathy, Myocardial ischemia
 Fluid management

• Anticoagulation management : Unfractionated heparin 100IU/kg prior to cross

clamping of aorta
• Fluid and transfusion management : goal directive fluid therapy using TEE and
dynamic parameters to assess intravascular volume status
• The goal is to maintain normal volume and optimal cardiac output
 Fluid management

• If urine output is <0.5ml/kg/hr before aortic cross clamping or after unclamping

potential causes are assessed and treated
• Evidence of hypovolemia treat with fluid
• Evidence of ventricular dysfunction treat with ionotrope
• Avoid colloids
 Blood salvage and transfusion

• Use of cell saver to minimise allogenic transfusion

• Tranfusion trigger 9gm/dl in case patient has severe or unstable ischemic heart
disease, evidence of cardiac or other organ ischemia or ongoing bleeding
• In case of significant bleeding transfusion of blood products in 1:1:1 ratio of RBC’s,
FFP and platelets
 Hemodynamic management
• Maintain systolic and mean BP within 20% of the patients baseline
• Hypotension : cause insufficient myocardial, cerebral and renal perfusion
• Severe hypertension : cause myocardial ischemia, increase surgical bleeding or aneurysm
rupture
• Cause of heamodynamic instability
• Aortic cross clamping
• Aortic unclamping
• Blood loss with hypovolemia
• Vasodilation due to combined effect of epidural and general anaesthesia
• Sympathetic stimulation with intubation during induction and extubation during
emergence
Physiologic changes with aortic cross-
clamp placement. Typical
hemodynamic response to aortic cross-
clamp placement. The level of cross-
clamp placement, changes in circulating
blood volume, depth of anesthesia
and/or anesthetic agents employed, and
other physiologic factors may have
varying effects.
 Hemodynamic effects of aortic
• Depends on cross clamping
•

1 Site of clamping : more in c/o supra celiac clamping than infrarenal clamp
2 Cardiac function of patient : coronary reserve, ventricular function
3 Effect of anesthetic drugs
4 Effect of splanchnic circulation venous tone : important in infrarenal/ infra
celiac clamping
 Role of site of clamping
• An increase in MAP and systemic vascular resistance (SVR) caused by impeded
arterial flow is the most consistent response to AXC, with an increase in arterial
pressure of 10% or more with infrarenal aortic cross-clamping. 2

• The potential for a substantially greater increase exists if the aorta is clamped at a
higher level such as above the celiac axis where flow to the abdominal viscera is also
interrupted.
 Infra celiac clamping
• The hemodynamic effects of an aortic cross-clamp below the level of the celiac axis
allows for shifting of blood flow to the splanchnic circulation, which in turn
augments its venous capacitance
• The typical result of this volume redistribution is little change in venous return and
cardiac output, unless major swings in splanchnic venous tone occur
 Supra celiac clamping
• When the clamp is placed above the celiac artery, the splanchnic circulation cannot
serve as a reservoir
• Rather, venous capacitance below the clamp decreases, expelling blood from the
splanchnic system to the central circulation, with resultant increases in filling
pressures and venous return
• The redistribution of blood volume in this setting is also affected by blood loss, fluid
loading, anesthetic depth, and administered vasopressors
Changes in blood volume distribution during aortic cross-clamping (AXC). The shifting
of blood volume with aortic cross-clamping is dependent on the level of cross-clamp
 Role of cardiac status
• Baseline myocardial contractility reserve may also affect the response to AXC during
AAA repair
• The increases in preload and afterload acutely increase myocardial work and
oxygen demand, particularly with supraceliac clamping
• The physiologic response to this increased demand is to increase myocardial
perfusion via coronary vasodilation
• P atients without significant CAD and preserved ventricular function may tolerate
P

these increases in preload and afterload with minimal effect on cardiac output
 Role of cardiac status
• In the setting of concomitant CAD where the coronary vasculature is already
maximally vasodilated and/or there is left ventricular dysfunction, the acute increase
in myocardial oxygen demand during AXC may precipitate myocardial ischemia,
overt heart failure, or both
 Hemodynamic management
during AXC
Goal : decrease afterload & LV wall stress with arteriolar dilators and normalizing
preload with venous dilators

Short-acting vasoactive agents (such as sodium nitroprusside, nitroglycerin, nicardipine

and/or clevidipine) are titrated to achieve these hemodynamic goals
 Hemodynamic management
during AXC
Because myocardial ischemia and/or heart failure may present acutely during this
critical period, agents to improve myocardial oxygen supply as well as inotropic
agents should be available to support ventricular function as necessary

Close communication between the surgical and anesthetic teams is paramount so that
pathophysiologic derangements can be anticipated and appropriately managed
Physiologic changes with aortic
cross-clamp release. Typical
hemodynamic response to aortic
cross-clamp release.
 Hemodynamic effects of
Unclamping
After completion of the entire AAA repair, release of the distal aortic cross-clamp is
frequently associated with dramatic hypotension

The mechanism for hypotension is multi- factorial

Distal aortic unclamping results in an immediate and profound (up to 70–80%) decrease
in SVR d/t tissue hypoxia & release of vasoactive mediators
 Hemodynamic effects of
Unclamping
sequestration of blood distal to the aortic cross-clamp, resulting in a relative central
hypovolemia

vasoactive and inflammatory mediators (such as lactic acid, oxygen free radicals,
prostaglandins, endotoxins, and cytokines) promote vasodilation and myocardial
depression on release of the aortic cross-clamp
 Management of hemodynamic
effects
Minimize ischemic time
of unclamping
Release the aortic cross-clamp gradually

Adequate volume loading

Discontinue vasodilatory agents

Start vasopressors

A slow release of the aortic cross-clamp and/or opening of iliac artery clamps one at a
time may allow for a more gradual metabolic washout with less profound hemodynamic
derangements
Mobilization of aortic cross-clamp during open abdominal aortic aneurysm repair. To
minimize unnecessary ischemic time on visceral organs, the aortic cross-clamp is moved
sequentially lower on the graft as each anastomosis is completed. Each cross-clamp
release will result in metabolic washout to the previously ischemic organs, although the
subsequent quick replacement of the cross- clamp lower on the graft will mitigate some
(D) Right renal artery is anastamosed, with perfusion to right kidney achieve by moving
aortic crossclamp distal. (E) Reperfusion of legs: all arterial clamps are removed.
Anaesthetic considerations for EVAR
 Anesthetic goals in EVAR
(a) To provide hemodynamic stability, and preserve perfusion to vital organs including
the brain, heart, spinal cord, kidney, and splanchnic vessels

(b) to avoid imbalance in myocardial oxygen supply and demand

(c) maintenance of intravascular volume and early identification and management of

bleeding

(d) normothermia
 Anaesthesia for EVAR
local anesthetic infiltration with sedation, regional,or general anesthesia.

Short infra‑renal endovascular procedures can be performed under local anesthetic

infiltration with sedation

Regional anesthetic techniques can be spinal, epidural or combined

spinal/epidural[CSE]

CSE gives a fast and dense block, and also allows top ups via the epidural in prolonged
procedures and can provide good postoperative analgesia
 Anaesthesia for EVAR
The main advantages of regional anesthetic techniques are less stress response, less
inflammatory response, avoidance of mechanical ventilation in a patient with
severe cardio vascular and pulmonary diseases, and good postoperative analgesia.

Things to consider when selecting a technique are patient’s premorbid states, the
length of the procedure, the use of anti‑platelets and anti‑coagulant medications,
and the ability to stay supine position throughout the procedure
 Benefits of GA in EVAR
General anesthesia is frequently more practical than regional anesthesia for the
following reasons:

• These patients are frequently on antiplatelet medications preoperatively and will

definitely require heparin intraoperatively. This might present a problem for regional
anesthesia

• Blood pressure control is easier and can be achieved by titration of anesthetic agents
and vasopressors in majority of case

• If aneurysm rupture occurs during the procedure, the patient’s airway is already secure
and transport to theater is less complicated
 Benefits of GA in EVAR
Breath‑holding on the ventilator is easy and can be prolonged if necessary to improve
the image quality in digital subtraction angiography

• Use of iliac bifurcated devices or complex fenestrated grafts and or concomitant open
surgery like femoro‑femoral crossover graft may take lengthy periods of time, which
may be tolerated poorly by some patients.
 Conversion from LA to GA
Pain and discomfort from enlarging hematoma and endovascular manoeuvring

Ventilatory compromise secondary to diaphragmatic splinting from expanding

hematoma

Ischemic pain in the buttocks and legs if the internal iliac artery and femoral artery
respectively are occluded

Metabolic disturbances and cardiovascular instability can cause intraoperative delirium

and restlessness

Some times secondary procedures such as embolectomy and femoral‑femoral crossover

grafting may be necessary
 Renal protection in EVAR
Incidence of renal dysfunction : 3 to 11%
Adequate hydration
Minimise contrast load
Avoid and stop nephrotoxic drugs
No role of N- Acetylcysteine
Mannitol : osmotic diuresis, free radical scavenger
No role of diuretics, dopamine
Fenodopam : renoprotective
 Blood pressure control in EVAR
• Deliberate Hypotension at time of stent deployment
• Minimal hemodynamic changes
• Hypertensive episodes - can be controlled with labetolol or metoprolol
• SPINAL CORD PROTECTION :
• Minimise duration of procedure
• Maintain cardiac output, augmentation of arterial pressure
• Hypothermia
• CSF drainage
• Steroids
 Special complications in EVAR
• POSTIMPLANTATION SYNDROME :
• Fever, leucocytosis, elevated inflammatory markers, but no evidence of sepsis
• Self-limiting, settles in 2 weeks
• Rule out sepsis, mainstay Rx : antipyretics, iv fluids
• ENDOLEAKS :
• TYPE I & III - needs to be reintervened
• Type II : settles within months after thrombosis of aneurysmal sac
 Classification of endoleaks
• Type I endoleak results from inadequate seal from the proximal or distal end of the
endograft.
• Type II endoleak is caused by inflow from a visceral vessel.
• Type III endoleak occurs as a result of a defect in the graft, a disconnection of modular
graft components, or an inadequate seal.
• Type IV endoleak occurs as a result of porosity of the graft fabric.
• Type V endoleak, also known as endotension, is an elevation in aneurysm sac pressure
without a demonstrable source of endoleak.
 Endoleak

Classification of endoleak. Type I endoleak results from inadequate seal from the
proximal or distal end of the endograft. Type II endoleak is caused by inflow from a
visceral vessel. Type III endoleak occurs as a result of a defect in the graft, a
disconnection of modular graft components, or an inadequate seal. Type IV endoleak
occurs as a result of porosity of the graft fabric. Type V endoleak, also known as
 Intraoperative Neurologic
Monitoring for Abdominal
Incidence of spinal cord injury < 1%,

Aortic Aneurysm Repair

increase in risk with suprarenal clamping, prolonged clamp times, release of micro emboli,
prolonged hypotension, anemia, emergency surgery, rupture, dissection
Prevention : avoidance of above risk factors
Lumbar drain placement with ICP goal - 10mmHG & mean arterial pressure
augmentation with MAP of least 70–80 mm Hg to maintain a spinal cord perfusion
pressure higher than 60 mm Hg
spinal cord monitoring with SSEPs, motor- evoked potentials, or both
Lumbar drain to be placed only in c/o anticipated neurologic insult post
 Post operative complications
The Society for Vascular Surgeons registry has recently reported an 11% perioperative
rate of major adverse events after AAA repair, including death, stroke, MI, renal failure,
respiratory failure, and paralysis; the overwhelming majority were death and MI. MI
rates of 5–10% for open AAA repair

Pulmonary complications: pulmonary infection - 17% due to mechanical ventilation ;

after EVAR - reported incidence of 3–7%. Lung protective ventilation, incentive
spirometry, bronchodilators, pulmonary toil letting helps
Renal dysfunction : incidence - 10-20% after open AAA repair with a risk of renal
replacement therapy of 1–3%.Although perioperative renal failure after EVAR has a
reported incidence of up to 10%

Bleeding : 1% ,causes includes : anastomotic leak, back-bleeding from arterial

collaterals, raw- surface oozing, dilutional coagulopathy, hypothermia, and circulating
anticoagulants
Intestinal ischemia : 1–3% of endovascular cases and up to 9% of open cases. Treatment
options range from aggressive resuscitation and broad-spectrum antibiotics for limited
disease to emergency bowel resection for full-thickness infarction or evidence of shock

Spinal cord ischemia is a relatively rare

Lower extremity ischemia :Technical issues with surgical anastomoses, acute thrombosis,
acute embolic disease, and clamp injury may all be a source for lower extremity ischemia.
Prevention by Adequate intraoperative systemic anti- coagulation and meticulous
surgical technique, distal aortic perfusion by shunt or temporary graft
Thank you for kind attention