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 : de inition, classi ication
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 ield 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

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 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 pro ile that the patient & caregivers can use in
making treatment decisions that may in luence 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 in luence patient care.

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 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 :

lipid-lowering, anti-in lammatory, plaque stabilising, antioxidant properties

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

OHA :

hold prior to sx to prevent hypoglycaemia under GA, especially METFORMIN- cause lactic
acidosis in the setting of hypovolemia and iodinated contrast agents used in vascular surgery

Shift to Insulin

 Abdominal aortic aneurysm

An aneurysm is typically de ined 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 in luence 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

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 Classi ication
Abdominal aortic aneurysms (AAAs) are classi ied 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.
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 Crawford classi ication of thoracoab- dominal aortic aneurysms

• De ined by anatomic loca- tion and the
extent of involvement.
• 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;
• Type IV aneurysms involve all or most
of the abdominal aorta, including the
visceral segment.
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 Etiology
Degenerative : most common etiology

In lammatory

Infective

Trauma

Congenital conditions

connective tissue disorders

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

While in lammation and macrophage in iltration 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
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 Epidemiology of AAA
AAAs are typically seen in older adults with an incidence that increases
signi icantly 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
modi ication

Nonmodi iable risk factors for AAA : age, gender, and family history

Modi iable risk factors : smoking, obesity, hyperlipidemia, hypertension, &

atherosclerotic arteriopathy (including CAD)

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 Epidemiology of AAA

Smoking is the modi iable 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 calci ication, preventing aneurysm formation

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 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 AAA1

Furthermore, the frequency of surveillance imaging for patients with

known AAA is a function of aneurysm size

 Indications for Abdominal Aortic Aneurysm Intervention

• The single 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, de ned 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 signi cant comorbidities.

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 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.

 Evidence for open repair V/S EVAR

EVAR provides a short-term survival bene it but no long-term survival bene it

No difference in either cardiac or aneurysm-related mortality between

groups at either intermediate- or long-term follow-up

Signi icantly higher rate of reintervention in the endovascular group,

although the majority of these reinterventions were endovascular-based
procedures associated with a low mortality rate
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Additional factors in luencing 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 calci ication,
or high thrombus burden.

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Additional factors in luencing surgical decision

Challenging iliac artery anatomy such as calci ication, 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

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Additional factors in luencing 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
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 Contraindications for EVAR

ABSOLUTE
Aortic neck diamater > 32 mm at the RELATIVE
More than 40% of the aortic neck
renal arteries: problem with adequate
diameter occupied with thrombus
proximal seal
Circumferential calci ication at aortic
Ruptured AAA with aortic neck length <
neck
7mm: at least 15 mm of undilated aorta
Aortic neck angulation > 60 degrees
below the renal arteries is ideal to
Bilateral iliac arteries < 6.5cm in
achieve an adequate seal between
diameter
endograft & aortic neck

 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

• In c/o proximal clamp prior to subclavian artery level, right radial artery cannulation

 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, luid
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 luids
• 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
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 Fluid management

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

cross clamping of aorta
• Fluid and transfusion management : goal directive luid 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 luid
• Evidence of ventricular dysfunction treat with ionotrope
• Avoid colloids
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 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 signi icant 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 insuf icient 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 cross clamping

• Depends on
Site of clamping : more in c/o supra celiac clamping than infrarenal
clamp
Cardiac function of patient : coronary reserve, ventricular function
Effect of anesthetic drugs
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 low 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 low to the
abdominal viscera is also interrupted.

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 Infra celiac clamping

• The hemodynamic effects of an aortic cross-clamp below the level of the

celiac axis allows for shifting of blood low 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
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 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 illing pressures and venous return

• The redistribution of blood volume in this setting is also affected by blood

loss, luid loading, anesthetic depth, and administered vasopressors
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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 placement (supraceliac vs infraceliac), release of catecholamines and administration of vasoactive medications, and overall blood volume.
•
 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 signi icant CAD and preserved ventricular function may tolerate these
P

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.
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 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 in lammatory mediators (such as lactic acid, oxygen free

radicals, prostaglandins, endotoxins, and cytokines) promote
vasodilation and myocardial depression on release of the aortic cross-
clamp

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Management of hemodynamic effects of unclamping

Minimize ischemic time

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

In case of profound hypotension, the aortic cross-clamp may be reapplied

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 of the
hemodynamic alterations. (A) Native aneurysm with right renal artery is shown. (B) Aortal and iliac arteris is clamped. Aneurysm sack is opened and right
renal artery is dissected. (C) Aorto-bifemoral graft with separate arterial graft is sewn in. Aortic clamp is moved from native aorta to proximal graft.
•
(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 identi ication and

management of bleeding

(d) normothermia

 Anaesthesia for EVAR

local anesthetic in iltration with sedation, regional,or general anesthesia.

Short infra‑renal endovascular procedures can be performed under local

anesthetic in iltration 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
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 Anaesthesia for EVAR

The main advantages of regional anesthetic techniques are less stress response,
less in lammatory 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
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 Bene its 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

de initely 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
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 Bene its 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.

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 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

 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 in lammatory markers, but no evidence of
sepsis
• Self-limiting, settles in 2 weeks
• Rule out sepsis, mainstay Rx : antipyretics, iv luids
• ENDOLEAKS :
• TYPE I & III - needs to be reintervened
• Type II : settles within months after thrombosis of aneurysmal sac

 Classi ication of endoleaks

• Type I endoleak results from inadequate seal from the proximal or distal end
of the endograft.
• Type II endoleak is caused by in low 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.
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Endoleak
 Intraoperative Neurologic Monitoring for Abdominal
Aortic Aneurysm Repair

• Incidence of spinal cord injury < 1%,

• 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 neurologic insult

 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

Thank you for kind attention