ANESTHESIA FOR

VASCULAR SURGERY
 Outline

Introduction
 Carotid endarterectomy ( CEA)

 Aortic surgery

 Endovascualr surgery

 Peripheral vascular surgery ( bypass

grafting)
 Vascular Surgery Patients
 Coexisting diseases:
 Age>70 yrs

 Hypertension

 Diabetes

 Smoking

 CNS: carotid disease, stroke

 Renal insufficiency

 Angina, CHF, prior MI or CABG

 50% of post op mortalities-MI

 General information
 Ischemic CVA-80%
 STROKE-thrombus, embolism, vasospasm
 Stroke: neurological deficit last >24 hrs
 TIA: neurological deficit resolve within 24 hrs
 Stroke in evolution: progressive worsening of symptoms
 Complete stroke: if territory completely affected
 Incomplete stroke: not completely affected
 Small emboli in ophthalmic arteries cause transient
monocular blindness( amurosis fugas)
 If MCA-C/L arm & face more involved
 If ACA-C/L leg more involved
Plaque Formation
 Physiological considerations
 Carotid disease is due to atherosclerosis
 Most common site is the bifurcation of vessels

 Ischemia is often due to embolic phenomenon

 During ischemia collateral flow critical

 Principal pathways : Circle of Willis, extra cranial

anastomotic channels, leptomeningeal
communications
 CBF: carotid 80% vertebral 20%

 CBF=CPP/CVR

 Auto regulation 50-150 mm Hg

CIRCLE OF WILLIS
 Indications for CEA
 Ipsilateral >70% stenosis in symptomatic
patients
 Severe ipsilateral stenosis in pt with
minor stroke
 30- 70% stenosis with ipsilateral
symptoms
 >60% stenosis in asymptomatic patients
 Preoperative evaluation
 CEA has an inherent risk of perioperative stroke and CVS events
 25% strokes associated with CEA occur intra-operatively
 33% mostly embolic; some homodynamic in origin
 Risk factors:
 active neurological process prior to surgical intervention
 Other risk factors for poor neurological outcome:
 Hemispheric vs. retinal TIA
 Left sided procedure
 Ipsilateral ischemic lesion on CT scan
 Contra lateral carotid occlusion
 Impaired consciousness
 Poor collaterals
 An irregular or ulcerated plaque
 CEA with CABG
 Uncontrolled HTN sys >180 & dia > 110mm Hg
 Pre-operative Assessment
 Good cardiac hx, previous MI, angina, exercise tolerance,
CHF, arrhythmias,
 Ecg, CXR, routine Echo and stress test may be indicated as well.
 Central nervous system: Pre-operative neurological deficits
 Cardiovascular system:
 CAD is present in about 20±40% of patients undergoing
CEA
 silent CAD: most influenced factor of long-term prognosis

 Continued: β-blocker / calcium channel blocker ( heart

protection)
 Discontinued: ACEI (lead to hypotension in combination with
anesthesia agents)& diuretics
 Monitoring
 Awake patient-
patient Gold standard
 EEG-
EEG Neurological changes .manage burst suppression
 SSEP-
SSEP not better than EEG, but more complex. May be a better indicator of
sub cortical ischemia
 Stump Press> 50 mm Hg.Hg estimate collateral circulation above cross clamp,
predict placement of temporary shunt.
 TCD( trans cranial Doppler ultra sound)
1. Assessing homodynamic ischemia,shunt function, embolic phenomenon,
hyper perfusion syndrome
2. Detect a significant decrease of velocity in the MCA during cross-clamping of the
ICA (the velocities decreased)
3. Detect embolization during and after CEA (sharp spikes)
 Oximetry-
Oximetry High false positive rate
 JvO2-
JvO2 Sensitivity,specificity and intervention thresholds not determined
 Carotid angiography- useful predictor of assessment of collateral circulation
 Others :measurements of CBF by xenon-133,transconjuctival O2 tension
 Choice of anesthesia
General anesthesia
Cervical epidural

Cervical plexus block( superficial &

deep)
Local anesthetic infiltration
 Anesthetic management
 Regional or general anesthesia-both can be used
 Technique should optimize
 perfusion to the brain,
 minimize myocardial stress & ischemia and
 allow rapid recovery
 Anesthetic:
 Barbiturates: no evidence for permanent focal deficits
 Volatile anesthetics: isoflurane best for cerebral protection
 Etomidate shown to worsen outcome in animal models
 Thiopental: shown to improve ischemic injury
 Propofol : rapid awakening
 Etomidate, thiopental, propofol-reduce cerebral metabolic rate
>CBF
 Muscle relaxant no direct effect
 Vasoactive agents: ephedrine, phenyepherine, dopamine
 General anesthesia
 GA not prevent hemodynamic response of manipulation of the
carotid sinus (severe vagal response)-leads to bradycardia & heart
blocks
 Treat with atropine I/V
 Advisable to inject 1-2 ml of 1% lidocaine in the tissue b/w
ICA & ECA before surgical manipulation but infiltration can
also cause bradycardia.
 Severe homodynamic response-spasm of the coronary artery
 Due to co morbidities (i.e. CAD, MI) important to avoid large BP
swings Especially upon intubation and emergence
 Heparin(5000-7500U I/V) prior to carotid clamping & protamine
50-150 mg prior to skin closure-reversal
 GENERAL ANESTHESIA
 Advantages
 Better airway & ventilation control
 Some cerebral protection

 Patient co operation not required

 DISADVANTAGES
 Expensive,less neurological monitoring
 Delayed post op neurological assessment

 Homodynamic instability
 Regional anesthesia
 Supplemental oxygen
 Benzodiazepines and/or opioids to make the
patient comfortable
 Propofol boluses may be needed

 Positiong
 Placed in supine position
 No head elevation
 Head tilted away from surgical site
 Shoulderroll may be helpful for exaggerated neck
extension
 Regional Anesthesia
 Deep Cervical Plexus Block
 Three separate injections
 Line drawn connecting the tip of the mastoid
process and the Chassaignac tubercle (i.e.
transverse process of C6)
 Another line drawn 1 cm posterior to the first
line; C2 transverse process lies 1 to 2 cm
caudal to the mastoid process
 22 G needle x3 advanced perpendicular to
the skin and slightly caudal until contacting
the transverse process (depth about 1.5 to 3
cm)
 If paresthesias elicited, inject 3 to 4 ml of
solution, if not elicited, walk along transverse
process in a caudal or cephalic direction

OR

 Inject in single injection at C4 transverse

process and rely on cephalic spread of the
anesthetic to C2 and C3 nerves
 Complications
 Intravascular injection
 Intrathecal injection

 Paralysis of the ipsilateral diaphragm

 Laryngeal block causing hoarseness,

coughing and dysphagia
 Regional Anesthesia
 Superficial Cervical Plexus block
 Anesthetize C2 to C4 branches
 Midpoint of the posterior
border of the
sternocleidomastoid muscle
 Injection of solution along the
posterior border and medial
surface of the muscle
 May block accessory nerve
causing trapezius muscle
paralysis
 Regional Anesthesia

 Bupivacaine (max. dose 3 mg/Kg)

 Longest duration of block
 Greatest cardiac toxicity
 Levobupivacaine
 Similar duration
 Less potential toxicity
 Expensive
 Ropivacaine ( max. dose 3 mg/Kg)
 Similar quality of block
 Shorter duration of postoperative pain relief
 GOAL: calm & co-operative patient
 Regional Anesthesia
 ADVANTAGES
 Superior neurological monitoring

 Cost effective( reduced need for shunt insertion, less hospital stay)

 Less homodynamic instability

 Reduced cardiac complications

 Less pulmonary complications

 Post op analgesia

 DISADNATAGES:
 Lack of airway control

 Cervical plexus complications( recurrent laryngeal nerve injury,

phrenic nerve injury ,Inadvertent intravascular injection)
 Patient co operation( uncomfortable position , claustrophobia)
 Modalities of cerebral protection
 Surgical- placement of a shunt during cross clamp
 Indications: if distal stump pressure<50 mm Hg
 Electrophysiological signs last> 10 min
 Physiologic:
 Mild hypothermia 33-34 degree centigrade
 normal to high BP( 10- 20% above normal)
 Treat hyperglycemia
 Treat intra op HTN( mild to moderate-nitroglycerine used
Marked- nitropruside dose50-100 mcg/Kg –beneficial effects on
coronary circulation. B blockers-cautiously. I/v nicardipine 0.25-
0-5 mg/Kg-protect focal ischemia)
 Hemodilution
 Maintenance of normocarbia
 Heparanization 75-100 U/Kg
 Cerebral protection
 Why is it important?
 Once compromise is discovered (or predicted) carotid shunt can improve
cerebral oxygen delivery
 Carotid shunt can be placed in both ECA or ICA; however ICA-more effective

 Why not shunt everyone?

 Potential displacement of atheromatous debris, introduction of air embolism or
thrombosis of shunt
 Kinking/obstruction

 Increases surgical time & cost

 Presence of shunt makes surgical field less than optimal

 Awake patient -gold standard neurological monitoring

 Assessment of grip strength of the contra lateral hand

 Responsive to verbal commands

 Same anesthesiologist for assessment in comparison of before and after cross

clamping
 Cerebral protection
 Maintenance of normocarbia
 Hypercarbia leads to cerebral vasodilatation
 Steal syndrome could occur

 Hypocarbia leads to vasoconstriction

 Ischemia to compromised area of brain

 Mild hypothermia (33-34ºC)-beneficial for cerebral

ischemia
 Suffer shivering in the recovery phase if mild hypothermia is
employed
 Consequent increase in myocardial oxygen consumption
 Routine employment of mild hypothermia is not recommended
 Endovascular cooling and rewarming devices.
 Hyperthermia should be avoided.
 Recovery & Complications
 The objective is a smooth and prompt emergence with optimal
systemic and cerebral hemodynamic & 24 hrs stay in ICU
 Additional problems as follows:
 Hypertension( surgical denervation of carotid baroreceptor)
 Post op hyper perfusion syndrome
 Blunting of ventilatory derive to hypoxemia (denervation of carotid body)
 Stroke, usually embolic, MI
 Bleeding & neck hematoma
 Cranial Nerve injury-hypoglossal, vagus, recurrent laryngeal, accessory,
glossopharyngeal, phrenic nerve-10%
 Unilateral damage- no immediate intervention
 Bilateral damage could result in upper airway obstruction
 Beware of patients with pre-existing neck surgery
 Hyper perfusion syndrome
 Abrupt increase in blood flow :35%
 Loss of auto regulation in surgically reperfused brain
 High risk : B/L high grade carotid artery stenosis,
U/L high grade stenosis with poor collateral, U/L
complete occlusion with contra lateral high grade
stenosis, severe hypertension after CEA
 Finding: headache, signs of transient cerebral
ischemia, seizures, brain edema and even
intracerebral hemorrhage
 Normotension should be maintained in patients at
risk for the hyper perfusion state
 Treatment: BP control, symptomatic
 Aortic Surgery
 Aneurysms
 Dissection
 Occlusive disease
 Trauma
 Coarctation
 Risks
 Most often requires CPB
 Large blood losses

 Hypertension pre-op, hypotension intra-op

 Myocardial ischemia

 Renal ischemia

 Spinal ischemia

 Death
Aorta & its branches
 Division of aorta
 Ascending-between aortic valve &
innominate
 Arch- between innominate & left
subclavian
 Descending- distal to left subclavian artery
but above diaphragm-descending thoraic
aorta & if below diaphragm-abdominal
aorta
 Aneurysms
True aneurysm
Involves dilation of all 3 layers of the vessel wall:
 (outer) Tunica externa - fibrous connective tissue
 (middle) Tunica Media- smooth muscle/elastic tissue
 (inner) Tunica interna - epithelial layer, squamous cells

False aneurysm
Caused by disruption of 1 or more layers of the vessel wall.
 Thoracic aortic aneurysms
 Rupture-death risk. >6cm. 50% rupture within one year.
 Surgical repair 2-5% mortality risk
 Leaking = >50% mortality
 Thoracic aneurysms: tracheal &/or bronchial compression/deviation,
Laryngeal nerve compression
 Crawford’s classification:
 Aneurysm of descending aorta distal to sq vein, ending above the origin of visceral
vessels.
 Aneurysm from the origins of subclavian artery to distal abdominal aorta.
 Aneurysm from the mid-descending thoracic aorta to distal abdominal aorta.
 Aneurysm from the diaphragm down to the distal aorta.
 Associated with atherosclerosis, connective tissue disorders
(marfan’s syndrome), congenital abnormalities, trauma, infection
(syphilis), HTN.
 Abdominal Aortic Aneurysm
 Common in older adults >60 yrs (5-7%)
 Genetic link
 Usually occurs in people with atherosclerosis.
 Symptoms: abdominal, groin, back pain,
syncope, flank mass, or paralysis
 Diagnosis: routine physical findings, abdominal
ultrasound.
 Abdominal Aortic Aneurysm
 Incidence
 Male: Female = 5:1
 Characterized
 Suprarenal
 Juxtarenal
 Pararenal
 infrarenal
 90-95% of AAAs involve the infrarenal abdominal aorta.
 Depending on size:
 4-5cm– elective repair with low operative risk and good life
expectancy.
 5-6 cm– need repair (mortality rate 0.9-5%)

 6-7 cm– threshold for rupture (mortality as high as 75%).

 Co arctation of aorta
 Narrowing of the aorta commonly just distal to the origin
of the left subclavian artery
 Occurs in the region of the ligamentum arteriosum.
 Preductal (infantile)-narrowing proximal to opening of
ductus. recognized early due to marked difference in
perfusion of upper & lower half of body
 Postductal( adult)-recognized late
 Lesion depend on
 severity of narrowing
 extent of collateral circulation
Co arctation of aorta
 Aortic dissection
 An intimal tear allowing blood to be forced into aortic wall
(media) or hemorrhage in media that extends & disrupts
aortic intima.
 Primary degenerative process-medial cystic necrosis. Tear
in the intimal layer, followed by formation and propagation
of a subintimal hematoma.
 Common-connective tissue disorders, hemorrhage in
plaque or cannulation site following cardiac surgery.
 STANFORD CLASSIFICATION:
 Type A involves the ascending aorta (DeBakey types I and II);
 Type B does not (DeBakey type III).
 Aortic Dissection

 DEBAKEY CLASSIFICATION:
 Type I involves the ascending aorta, aortic arch, and descending
aorta.
 Type II is confined to the ascending aorta.
 Type III is confined to the descending aorta distal to the left
subclavian artery.
 Proximal dissection-surgically
 Distal-may be medically
 Aim is to reduce
 systolic BP(90-120 mm Hg)
 aortic wall stress by I/V nitropruside, b blockers,labetalol
 If dissection progresses, may develop aortic insufficiency,
coronary ischemia, cerebral infarction, occlusion of limb
circulation, cardiac tamponade
Cross clamping pathyphysiological effects
 Homodynamic Response to Aortic Cross-clamping
 Increased Impedance
 Blood Volume Redistribution
 Oxygen Consumption
 Coronary Blood Flow and Myocardial Contractility
 Response to Unclamping
 Role of Humoral Factors
 Acidosis
 Renin-Angiotensin System
 Catecholamine and the Sympathetic Nervous System
 Oxygen Free Radicals
 Prostaglandins
 Platelets and Neutrophils
 Anaphylatoxins and Complement Activation
 Endotoxins, Cytokines, and Other Mediators
 Before Clamp
 Appropriate monitoring
 Thoracic epidural
 IHD-safe induction
 Upper-body warming
 GTN infusion
 Vasopressors/ Inotropes
 Relative fluid restriction
 Permissive hypotension
 Heparin
 Kidney protection( fluids, dopamine, mannitol, N-acetyl cysteine
NACC)
 Cooperate with surgeon as clamping time approaches
 X clamp: increased impedence

 MAP  50%
SVR 
 HR =
 CO/CI  (or  or =)
 LVESV  70%

 CVP/PCWP  40%
 LVEDV  30%
 X-Clamp Blood Volume Redistribution
(BVR)
 x-clamping of thoracic aorta
 Afterload  Cardiac dimensions
 “Blood transference” from lower to upper body  “Systemic
flow”

 BVR between compartments (determined by time constants)

 arterial to venous blood flow  intramural venous
pressure
 elastic recoil  splanchnic venous vasculature collapses
 venous capacitance  venous return  cardiac output
 X-CLAMP OXYGEN CONSUMPTION
 MRO2 distal to X-Clamp
 Proximal O2 uptake (paradoxical)
 sympathoadrenal discharge
 microcirculatory disturbances 2 to:
 Hypervolemia

 Vasodilatation

 flow

 AV shunting
 effect starts immediately after XC
 Total BMRO2 + SvO2 and CvO2 (O2 uptake above XC)
 X-CLAMP: coronary blood
flow/myocardial contractility
 Afterload  contractility  CBF

 Pre­load (2 to BVR)  LVEDP

 CPP = DAP – LVEDP

 Even with normal coronary vessels cardiac MRO2 is not always

met by myocardial O2 supply if LVEDP restricts coronary blood

flow
 Unclamp: Hemodynamic Effects
 MAP/SVR  70-80%
LVEDP 
 CO/CI  (or  or =)
 CVP/PCWP  40%
 LVEDV  30%
 LVESV  70%
 Systemic hypotension
 central hypovolemia: sequestration of blood in reperfused organs
 BVR reversal  splanchnic volume 
 hypoxia-mediated vasodilatation  vascular capacity 
 vasoactive and myocardial-depressant metabolites from ischemic tissue
 Pulmonary hypertension (PAP  PCWP  CVP )
 vasoactive metabolites
 cardio depressant mediators
 Measures to reduce effects
 Heparin
 ischemia-reperfusion injury (IRI)
 neutrophil adherence (2° to negative charge)
 antiplatelet and anti-inflammatory properties
 activation of complement
 Pentastarch/Hetastarch
 cerebral IRI
 pulmonary damage
 Mannitol
 neutrophil oxidative bursts  H2O2 production
 ischemia-reperfusion injury (IRI)
 Epidural anaesthesia
 C3a and C5a (? Direct effect of LA e.g. membrane-stabilization effects)
 Gradual release of Clamp
 IRI if O2 delivery during reperfusion (? reperfusion with hypoxic blood 
micro vascular injury)
 GTN & shunts
 decrease preload & myocardial benefits
 During Clamp
 Maintain circulatory volume
 Increase fluid requirement-10-12 ml/Kg/hr( large incision, extensive
dissection)
 Average blood loss 4 units
 Suckers & swabs; Hb measurement
 Blood salvage
 CVP/PCWP
 Arterial waveform
 Cross-clamp duration <30 min
 Infra-renal
 Supra-renal
 Unclamping
 Cooperate with surgeon
 One leg at a time
 Replace clamp if severe hypotension
Renal protection (fluids& mannitol)
 Etiology of ARF
 pre-renal azotemia
 ATN 20 (i) ischemia & (ii) nephrotoxins
 Kidneys receive 20 – 25% CO
 Autoreg RBF & GFR at MAP 85 – 180mm Hg
 MAP 60 –70 is on steep descent part curve
 HTN right shifts curve
 Maintain adequate cardiac function
 Mannitol: increase tubular flow & “wash out” debris.
 Decrease Na-K- Cl pump , medullary O 2 requirement
 Dose:0.5-1g/Kg.Effect In 5-15 min with peak in 30-45 mins
 High dose may cause ARF
 Dopamine & NACC
 Low dose stimulate DA-1 & DA-2 receptors
 renal a. vasodilation  RBF
 Na reabsorption
 Morbidity:tachyarrhythmia,ischemia
 NACC
 Antioxidant useful in acetaminophen toxicity
 Initial role in prevention of contrast nephropathy
 No benefit in preventing ARF in infrarenal aortic
Stenosis in pts with normal renal function
 Fenoldopam

 Pure DA-1 agonist not available

 In animals preserves RBF during hypotension
under GA
 Maintain Creatinine clearance & decrease in BP
infrarenal aortic stenosis pts
 Infusion dose:0.01-1.6 mcg/Kg/min
 Anesthetic management
 Ascending Aorta:
 Similar to cardiac surgery utilizing CPB
 Consider fem-fem bypass( sternotomy may rupture
aneurysm)
 Special considerations:
 Long aortic cross clamp times
 Large blood loss( use aprotinin)
 Left radial Arterial line-clamping of innominate artery
 Nitropruside for BP control
 In aortic dissection- 1.5 mg/Kg lidocaine &B blockers
(esmolol 1mg/Kg for tachycardia & HTN), cannula for CPB in
femoral artery
 Anesthetic management
 Aortic Arch:
 Similar to cardiac surgery utilizing CPB -median
sternotomy with deep hypothermic cardiac
arrest
 Goal- cerebral protection
 Hypothermia to 15 degree centigrade
 Thiopental infusion( Maintain flat EEG)
 Corticosteroids
 mannitol
 Anesthetic management
 Descending Aorta:
 Usually without CPB
 L. thoracotomy incision
 One lung anesthesia
 PA catheter, arterial line( rt radial used as left subclavian
artery may be clamped), Many large bore I/V, TEE, Cell
saver, SSEP
 Cross Clamping issues:
 Acute HTN above clamp & hypotension below with
increase in LV afterload
 ↑SVR, myocardial ischemia, CHF, ↓CO, increase
LVEDP& V
 Limit fluids pre-clamping
 ↑anesthetic depth
 Nitroglycerine, nitroprusside used
 Anesthetic management
 Clamp Release issues:
 SEVERE RELASE HYPOTENSION,↓SVR, hyperkalemia
( abrupt release of clamp with reversal of effects & release of acidic metabolites from
ischemic lower body)
 Preload with fluids( crystalloid, colloid) before release,
 slow release of cross clamp
 vasopressor
 ABGs acidosis (bicarb, ↑min. vent.)
 Paraplegia risk due to thoracolumbar artery injury
 Renal failure
 Emergency Aortic Surgery Pre OP
 Large gauge peripheral IV cannulae
 Bloods: FBC, Coag, U&Es - don’t wait for results
 X-match: 10 units, FFP and platelets
 Brief history
 ECG?
 CXR?
 Cautious IV fluids
 correct hypovolaemia, improve BP & CO & organ perfusion
 raise BP, dislodge clot and overcome tamponade
 Preparation for Emergency Surgery
 16G or 14G IV cannulae
 Swan sheath
 Blood & crystalloid / colloid – pressurised, warmed
[O negative if no X-matched blood]
 One or both arms out on boards
 Etomidate, fentanyl, sux, non- dep relaxant
 Metaraminol 0.5 mg/ml/ Phenylephrine 100 mcg/ml, Adrenaline 1:100 000,
Atropine
 Arterial line( if time permits)
 Urethral catheter
 CVP [usually inserted during operation]
 Thoracic epidural
 Induction & Maintenance
 2 Anaesthetists
 Surgeons scrubbed; abdomen prepped & draped
 Blood and fluids ready to infuse rapidly
 Pre-O2 & cricoid pressure

 Fentanyl, etomidate, suxamethonium

 If patient in shock, let surgeons start as soon as anaesthesia is induced.
 Aim to avoid catastrophic drop in BP but not to restore a normal BP until the aorta is
clamped
 O2 & gentle IPPV if very low or unrecordable BP

 Opioids +++
 Maintain with volatile or propofol
 Remember non-depolarising relaxant
 Aortic clamping
 Hopefully below renal arteries
 BP may rise to normal levels in a previously shocked
patient
 If BP was normal until now, hypertension is likely to
develop when the aorta is clamped
 Treatment of hypertension
 deepen anaesthesia
 GTN infusion
 SNP infusion
 Esmolol
 Renal protection
 No good evidence that mannitol, frusemide or
dopamine reduce the incidence of acute renal
failure
 Hemodynamic optimisation peri -operatively
 Dopamine may cause myocardial ischaemia even
at “renal” doses
 Mannitol may have other beneficial effects
 Further management
 CVP catheter (+ Swan sheath + PA catheter)
 Temperature probe
 Nasogastric tube
 Once aorta is clamped, aim for normal BP, CVP, (PCWP)
 Transfuse to keep Hb > 85 g/l
 Treat coagulopathy
 Primarily DIC
 Prolong coag times and thrombocytopenia are common
 Lab results too slow to aid management
 Request FFP and platelets pre-op
 Give Platelets, FFP ± Cryo after aorta is clamped
 Post op care
 Transfer to ITU asleep, ventilated, monitored and
covered
 Correct hyper- or hypotension
 Sedation and analgesia – eg propofol( 50-200
mcg/Kg/min) and alfentanil infusions( 0.5-3 mcg/Kg/min)
 Continue warming if hypothermic
 Ventilate until warm, normovolaemic, acidosis resolved,
well oxygenated
 Aim for Hb > 85 g/l and no severe coagulopathy
 Complications
 Continuing haemorrhage
 Myocardial ischaemia & infarction
 Cardiac failure
 Respiratory failure
 Renal failure
 Lower limb ischaemia
 Large bowel ischaemia
 Infection
 Stroke; paraplegia
 Spinal cord-paraplegia
 Low thoracic levels dependant on variable blood supply( vertebral,
thoracic & abdominal aorta)
 More if X clamping time>30 min, extensive surgery & emergency
procedure.
 Risk: Anterior fibers > posterior( anterior spinal artery syndrome-loss of
motor & pinprick sensations but preserve vibration & propioception)
 May be source of significant back bleeding when aorta opened
 Spinal cord protection: Decrease X-clamp time
 Avoid excessive reduction in BP above cross clamp
 Partial bypass with hypothermia or temporary heparin coated shunt
 Steroids & mannitol( decrease CSF production)
 Decrease spinal cord perfusion pressure (SCPP = MAP - CSFP) using drain
Longitudinal view of spinal cord blood
supply
Partial bypass

Needs heparanization
& CVT surgeon
 CSF drainage
 Indications:
 involvement T9-T12 (artery of Adamkiewicz)
 Involvement of arch vessels (origin ant. spinal a.)
 Previous TAA if AAA repair or vice versa
 Symptomatic spinal ischemia
 Complications:
 Subdural hematoma
 Meningitis
CSF drainage

Need 1.drainage bag

2.presuure monitors
 Endovascular Surgery
 Performed under local, GA, regional
 Radial a-line & IV’s in right arm
 Left arm & both groins used for surgical access
 No cross clamping
 Patients are discharged in 1-2 days post-op
 GA with muscle relaxation or combined spinal epidural
or only spinal
 Disadvantages:
 Endoleaks - (failure to exclude the AAA)
 Severe ischemic pain-I/V opioids
 Require follow-up with serial CT scans
 Demands more office visits than open
 Peripheral Vascular surgery
 Bypass grafting for occlusive disease or
aneurysms
 Upper or lower extremities

 Endogenous vessels or synthetic (Gortex)

 Anesthesia options:

 General

 Regional
 Peripheral Bypass
 Femoral- popliteal and lower;
 general, spinal, epidural

 Ileo -femoral and lower;

 general, spinal, epidural

 Axillo -femoral;
 General, regional, local
THANK YOU