Jurnal Internasional

European Journal of Cardio-Thoracic Surgery 47 (2015) 943–957 POSITION STATEMENT
doi:10.1093/ejcts/ezv142
Cite this article as: Etz CD, Weigang E, Hartert M, Lonn L, Mestres CA, Di Bartolomeo R et al. Contemporary spinal cord protection during thoracic and
thoracoabdominal aortic surgery and endovascular aortic repair: a position paper of the vascular domain of the European Association for Cardio-Thoracic
Surgery. Eur J Cardiothorac Surg 2015;47:943–57.
Contemporary spinal cord protection during thoracic and
REPORT
thoracoabdominal aortic surgery and endovascular aortic repair:
a position paper of the vascular domain of the European Association
for Cardio-Thoracic Surgery†
Christian D. Etza,‡, Ernst Weigangb,‡, Marc Hartertc, Lars Lonnd, Carlos A. Mestrese,f, Roberto Di Bartolomeog,
Downloaded from https://academic.oup.com/ejcts/article/47/6/943/355104 by guest on 10 October 2020

Jean E. Bacheth, Thierry P. Carreli, Martin Grabenwögerj, Marc A.A.M. Schepensk and Martin Czernyl,m,*
a
Department of Cardiac Surgery, Herzzentrum Leipzig-University Hospital, Germany and Mount Sinai School of Medicine, New York, NY, USA
b
Department of Vascular and Endovascular Surgery, Evangelisches Krankenhaus St. Hubertus, Berlin, Germany
c
Department of Cardiothoracic and Vascular Surgery, University of Mainz, Mainz, Germany
d
Department of Vascular Surgery and Cardiovascular Radiology, Faculty of Health Science, Rigshospitalet Copenhagen, Copenhagen, Denmark
e
Department of Cardiovascular Surgery, Hospital Clinic Barcelona, Spain
f
Heart and Vascular Institute, Cleveland Clinic Abu Dhabi, Abu Dhabi, United Arab Emirates
g
Department of Cardiovascular Surgery, Policlinico Sant’Orsola-Malpighi, Università di Bologna, Bologna, Italy
h
Nogent sur Marne, France
i
Department of Cardiovascular Surgery, Inselspital, University Hospital Bern, Bern, Switzerland
j
Department of Cardiovascular Surgery, Hospital Hietzing, Vienna, Austria
k
Department of Cardiothoracic Surgery, AZ Sant-Jan, Brugge, Belgium
l
Department of Cardiovascular Surgery, University Hospital Zurich, Zurich, Switzerland
m
Department of Cardiovascular Surgery, University Heart Center Freiburg — Bad Krozingen, Freiburg, Germany
* Corresponding author. Department of Cardiovascular Surgery, University Heart Center Freiburg — Bad Krozingen, Hugstetterstrasse 55, 79106 Freiburg, Germany.
Tel: +49-761-27028180; fax: +49-761-27025500; e-mail: martin.czerny@uniklinik-freiburg.de (M. Czerny).
Received 1 September 2014; received in revised form 14 January 2015; accepted 29 January 2015
Abstract
Ischaemic spinal cord injury (SCI) remains the Achilles heel of open and endovascular descending thoracic and thoracoabdominal repair.
Neurological outcomes have improved coincidentially with the introduction of neuroprotective measures. However, SCI ( paraplegia and
paraparesis) remains the most devastating complication. The aim of this position paper is to provide physicians with broad information
regarding spinal cord blood supply, to share strategies for shortening intraprocedural spinal cord ischaemia and to increase spinal cord tol-
erance to transitory ischaemia through detection of ischaemia and augmentation of spinal cord blood perfusion. This study is meant to
support physicians caring for patients in need of any kind of thoracic or thoracoabdominal aortic repair in decision-making algorithms in
order to understand, prevent or reverse ischaemic SCI. Information has been extracted from focused publications available in the PubMed
database, which are cohort studies, experimental research reports, case reports, reviews, short series and meta-analyses. Individual chap-
ters of this position paper were assigned and after delivery harmonized by Christian D. Etz, Ernst Weigang and Martin Czerny. Consequently,
further writing assignments were distributed within the group and delivered in August 2014. The final version was submitted to the EJCTS for
review in September 2014.
Keywords: Spinal cord injury • Surgery • TEVAR • Thoracic aorta • Thoracoabdominal aorta
BACKGROUND ischaemic spinal cord injury (SCI) remains the most devastating
complication after repair by any modality. In 1993, Svensson
Over half a century after the first successful surgery for aneur- described the risk of SCI after open surgery according to the
ysms of the descending thoracic aorta (DTA) and thoracoabdom- ‘Crawford classification’—15% of Type I, 31% of Type II, 7% of
inal aorta (TAAA) by Etheredge (in 1955) and De Bakey (in 1956), Type III and 4% of Type IV aneurysm patients suffered post-
operative SCI. In the past two decades, the neurological
† outcome of open DTA/TAAA repair has improved coincidentally
Presented at the 28th Annual Meeting of the European Association for Cardio-
Thoracic Surgery, Milan, Italy, 11–15 October 2014. with the introduction of several neuroprotective adjuncts and by
‡
The first two authors contributed equally to this work. cerebrospinal fluid (CSF) drainage [1–9]. In spite of numerous
© The Author 2015. Published by Oxford University Press on behalf of the European Association for Cardio-Thoracic Surgery. All rights reserved.
944 C.D. Etz et al. / European Journal of Cardio-Thoracic Surgery
strategies designed to reduce the risk of SCI, its occurrence is (with less robust collateralization when compared with the thor-
relevant [1, 3, 4, 10–15] (Tables 1 and 2). acic region where intercostal arteries (ICAs) provide instant back-
Thoracic endovascular aortic repair (TEVAR) offers a less- up flow originating, e.g. from both internal mammary arteries),
invasive approach diminishing the magnitude of repair-associated (iii) extended aortic cross-clamp times during open repair—
injury by avoiding thoracotomy and aortic cross-clamping, minim- particularly when adding prolonged (normothermic, or only mild-
izing perioperative end-organ ischaemia and the insult to the re- to-moderate hypothermic) distal circulatory arrest to segmental
spiratory system, but is still associated with a significant risk of SCI. inflow compromise [19–21], while deep hypothermic circulatory
In 2007, Coselli presented the largest series of open TAAAs so arrest (DHCA) and distal aortic perfusion might be protective
far of 2286 patients reflecting a significant improvement in spinal [19, 22–27] and (iv) perioperative hypotension [e.g. after weaning
cord protection with 3.3% for Type I, 6.3% for Type II, 2.6% for from CBP [28], or during the early postoperative period (e. g. during
Type III and 1.4% for Type IV TAAAs—the current benchmark for temporary atrial fibrillation) [29, 30]]—presenting a widely underesti-
endovascular repair. SCI is an individual disaster with a profound mated risk factor responsible for a significant number of cases of
impact on early mortality, longevity and healthcare cost, and postoperative ischaemic injury resulting in delayed-onset SCI: up to
eventually a significant socioeconomic issue [16, 17]. Conrad et al. 83% of all patients developing SCI after open repair and 87% of
[18] stratified SCI after open and endovascular DTA/TAAA repair cases after endovascular repair, respectively [19, 29, 31–35].

by deficit severity and determined its impact on early and late sur- After TEVAR and open repair, a ‘post-implantation syndrome’
vival: the 30-day mortality was significantly higher in patients with may aggravate the risk for delayed SCI [36]. Recent advances in the
SCI (and varied with the severity of the SCI); 5-year mortality understanding of the anatomy and physiology of the collateral
more than doubled with SCI and reached 100% among patients network supplying the spinal cord have led to a new experimental
with flaccid paralysis. strategy of the ‘staged repair’ [37, 38]. This strategy has been vali-
The final goal to eliminate SCI has not yet been reached. Since dated in a retrospective analysis, might be applicable to open and
ischaemic SCI is multifactorial in origin, contemporary spinal cord endovascular repair and might be particularly suitable for hybrid
protection requires an integrated strategy and a multimodality ap- repairs. Nonetheless, reoperative DTA/TAAA repair might be sig-
proach. The succesful treatment of the—often old and frail— nificantly safer with hypothermic circulatory arrest (HCA) for two
patient with extensive aortic pathology remains a challenge for all reasons: it protects the cord from intraoperative ischaemic insults
members of the multidisciplinary aortic team. by decreasing metabolism; secondly, it reduces the incidence of
Common risk factors for SCI after DTA/TAAA repair are the follow- postoperative haemodynamic instability resulting from intraopera-
ing: (i) Aneurysm extent—related to the number of segmental arter- tive visceral ischaemia [23, 25, 29].
ies (SAs) compromised, e.g. occluded, sacrificed or reimplanted Based on these considerations, contemporary concepts for
during repair, (ii) location—aneurysms affecting the lumbar region perioperative spinal cord protection involve the following: (i) the
maintenance of higher than normal arterial blood pressure values,
(ii) the drainage of CSF and (iii) the reattachment of critical SAs in
open repair (particularly if staging is not an option) [5, 13, 29, 39–43].
Table 1: Classes of recommendation
The prevention of spinal cord ischaemia requires the knowledge-
able use of these adjuncts and a thorough understanding of the
Class Definition
anatomy and physiology of spinal cord blood supply, the appro-
I Evidence and/or general agreement that a given treatment or priate monitoring modalities and the characteristics of haemo-
procedure is beneficial, useful, effective dynamic support, surgical and interventional techniques, and their
Suggested wording to use—is recommended/is indicated interaction.
II Conflicting evidence and/or divergence of opinion about the
usefulness/efficacy of the given treatment or procedure
IIa Weight of evidence/opinion is in favour of usefulness/efficacy
Suggested wording to use—should be considered INTRODUCTION
IIb Usefulness/efficacy is less well established by evidence/opinion
Suggested wording to use—may be considered Aortic disease, including DTA and TAAA, is the 12th leading cause
III Evidence or general agreement that the given treatment or
of overall death in the USA: between 43 000 and 47 000 patients
procedure is not useful/effective and in some cases may be
harmful die annually in the USA from diseases of the aorta and its branches
Suggested wording to use—is not recommended [44]. While the exact numbers for Europe are not readily available,
an estimated 110 000–125 000 Europeans die annually from aortic
disease. The natural history of DTA/TAAA is devastating and the
5-year survival rates range 13–50% [45–48]. The majority of patients
with DTA/TAAA are in their 60s, 70s and 80s and have difficulties in
tolerating the physiological insult of open surgical repair. In Europe,
Table 2: Levels of evidence probably fewer than 5000 (<2000 in the USA) DTA/TAAA per year
are treated, with a hospital mortality rate of up to 20% and a 1-year
Levels Definition survival rate of only 60–70%; as a consequence, probably 4 of 5
patients with DTA/TAAA decline or are not offered surgery because
A Data derived from multiple randomized clinical trials or
it is anticipated that they will have prohibitive operative mortality
meta-analyses
B Data derived from a single randomized clinical trial or large and morbidity.
non-randomized studies Open repair and TEVAR both severely compromise the blood
C Consensus of opinion of experts and/or small studies, supply to the spinal cord: by extensive SA sacrifice during surgery,
retrospective studies, registries the simultaneous SA occlusion with the deployment of covered
stent-grafts or the interruption of collateral perfusion during aortic
C.D. Etz et al. / European Journal of Cardio-Thoracic Surgery 945
cross-clamping (or with large-bore sheaths in place during pro- Electrophysiological assessment is helpful in detection of ischae-
longed endovascular procedures) leaving the hypogastric arteries mia in the monitored neural tracts, the use somatosensory evoked
not being perfused and the collateral network thus being deprived potentials (SSEPs) or motor evoked potentials (MEPs) and has
of its major distal inflow source. Accordingly, the major risk factors been studied extensively in thoracoabdominal aortic surgery and
for ischaemic SCI during TAA/A repair are the following: (i) the TEVAR. Additionally, these methods might be able to detect situa-
extent of aortic graft replacement or endovascular coverage (i.e. the tions of marginal blood flow resulting in neuronal dysfunction
REPORT
complexity of the repair), (ii) the presence of acute aortic dissection (i) at a time when the neurons are still salvageable and the insult is
—particularly, with extensive, acute SA malperfusion due to the for- potentially reversible and (ii) allowing for guidance of therapeuti-
mation of a false lumen and (iii) the degree of urgency (i.e. limited cal interventions to relieve acute ischaemia.
time for proper planning, no option for staging or perioperative
haemodynamic instability). The risk may vary in the range 4–7%
after TEVAR for DTA, 2–28% after elective descending aortic surgery SPINAL CORD BLOOD SUPPLY
and up to 40% after emergency repair of extensive TAAAs (Table 3).
The impact of prior distal aortic operations—i.e. abdominal Arterial blood supply to the spinal cord is provided by the anterior
aortic aneurysm repair—on SCI risk after reoperative surgery for spinal artery (ASA) arising cranially from both vertebral arteries to

more proximal aortic disease affecting the descending or the supply its anterior portion. A pair of posterior spinal arteries
TAAA has been the focus of controversial expert debates. (PSAs) also arising from the vertebral arteries supplies the poster-
Retrospective series suggest a decreased risk of acute SCI, also ior spinal cord. Caudally, the ASA receives arterial collateral blood
supported by experimental evidence and the concept of a ‘staged from the internal iliac arteries and the sacral arteries, and from the
repair’—while others discuss an increase in the risk of SCI [37, 38, inferior mesenteric artery. Additional supply is provided by paired
55–57]. The key to understanding the pathophysiology behind intercostal and lumbar SAs that originate from the DTA and ab-
reoperative repair might be to assess how the previous repair dominal aorta (Fig. 2A).
affected the collateral inflow—i.e. if the hypogastric arteries have Two different paradigms are used to explain the elusive nature
been sacrificed or the left subclavian artery has been overstented, of spinal cord circulation, one based on anatomical (direct, seg-
the risk during subsequent repair might be increased. mental supply) and the other on less anatomical and rather
The pathophysiology of SCI in DTA/TAAA surgery is essentially dynamic demand-depending (collateral) blood supply [42].
an ischaemia–infarction model caused by a variety of mechanisms A thorough understanding of the anatomy of the blood supply of
(Table 4). It has been assumed that injury arises primarily as a con- the spinal cord appears essential for developing strategies to
sequence of two mechanisms: (i) an intraoperative insult after prevent SCI. Direct visualization of these vessels is arduous and
temporary interruption of spinal cord blood supply during surgery most surgeons therefore continue to rely on a few classic anatom-
of duration sufficient to irreversibly damage cell bodies and nerve ical studies. The most influential of these has been the treatise
tracts in the spinal cord and (ii) the second insult was thought to by Albert W. Adamkiewicz (1850–1921), whose meticulously
occur postoperatively: permanent reduction in blood supply sec- detailed drawings suggest that the most important input to the
ondary to sacrifice of critical blood vessels—the thoracic (intercos- ASA is a single dominant branch of an SA in the lower thoracic
tal) and lumbar SAs—to a level incompatible with cord viability. or upper lumbar region, which is now often referred to as the
While the first pathomechanism primarily affects open surgical Artery of Adamkiewicz, who in 1881 published his thesis entitled,
repair, the second mechanism also limits endovascular repair due Die Blutgefaesse des menschlichen Rueckenmarks’ at the University
to the sudden simultaneous occlusion of SA inflow when a stent- of Cracow [59]. His concept became the accepted doctrine for over a
graft is deployed. In addition, perfusion to the hypogastric arteries century—and the rationale to justify reimplantation of intercostals
supplying distal collateral inflow may be compromised by large- and lumbar arteries in TAAA surgery—even after Guy Lazorthes in
bore sheaths during the procedure. Starting with aortic cross- 1971 postulated a new concept he had developed since the 1960s,
clamping or circulatory arrest during open aortic repair and based on three main arteries, each arising from several regional seg-
followed by the sacrifice or exclusion of SAs, arterial blood supply mental arteries, supplying the cervical, thoracic and lumbosacral
to the spinal cord is acutely reduced, possibly triggering oedema region of the spinal cord [60–62].
and subsequently an increased production of CSF (Fig. 1). Elevated The clinical relevance of these concepts is controversial: the
CSF pressure generates a gradient hindering arterial blood from opponents of Adamkiewicz argue that SA reimplantation during
entering the spinal canal, and arterial blood supply to the spinal TAA/A repair is the best possible strategy for preserving spinal
cord is progressively reduced leading to a vicious circle of progres- cord blood supply [63–68]. Despite various painstaking and in-
sive ischaemic SCI. ventive attempts to avoid ischaemic SCI with this approach, there
Significant progress has been made in understanding the para- continues to be a definite, seemingly irreducible incidence of SCI
spinous and intraspinal arterial collateral network supporting the after treatment of extensive TAAA [65, 68–70]. Furthermore, reat-
spinal cord during deprivation of major sources of direct arterial taching intercostal or lumbar SAs—a daunting undertaking during
blood supply [37, 58]. Contemporary strategies to prevent acute open surgical repair—is not possible with current endovascular
SCI in DTA/TAAA surgery or TEVAR primarily aim at minimizing techniques. (Table 3 summarizes the incidence of SCI after both
the duration of ischaemia during procedures by means of improv- open surgical and endovascular repair.)
ing perfusion pressure and flow as well as tissue oxygen delivery, Imaging techniques to identify SAs are considered critical to
and enabling early detection of spinal cord ischaemia to permit spinal cord function are controversial. In the 1990s, selective inter-
immediate intervention (Table 5). Intraoperatively, numerous costal angiography was introduced to preoperatively identify the
adjuncts have been implemented to reduce SCI. Currently, left Artery of Adamkiewicz [63, 65]. Then, radiological imaging tech-
heart bypass (LHB), CSF drainage, reimplantation of the most im- nology evolved and Nojiri et al. [71] proposed preoperative detec-
portant SAs, hypothermia and maintenance of an adequate mean tion of the Artery of Adamkiewicz using intra-arterial computed
arterial pressure (MAP) are thought to be effective measures. tomographic angiography. Recently, it became possible to identify
946
Table 3: Contemporary incidence of ischaemic SCI with permanent dysfunction according to aneurysm extent—reported by international centres of excellence in endovascular
(TEVAR) and open surgical aortic repair

Year N Incidence of ischaemic SCI with permanent dysfunction
according to aneurysm extent
DTA (%) Thoracoabdominal/Crawford (%) Technical/perioperative management
Type I Type II Type III Type IV Segmental arteries CSF drainage Neuromonitoring
Endovascular (TEVAR)
Greenberg et al. [32] 2008 352 1 10 19 5 3 Occluded Yesa None
C.D. Etz et al. / European Journal of Cardio-Thoracic Surgery

b b b b
Gravereaux et al. [49] 2001 53 5.7 Occluded Yes, with extensive coverage None
b b b b
Conrad et al. [18] 2008 105 7 Occluded Yes None
b b b b
Bavaria et al. [50] 2007 140 3 Occluded Not consistently None
b b b b
Feezor et al. [51] 2008 326 10 Occluded None in most patients None
Stone et al. [52] 2006 74 10.4c b b b b
Occluded d
None
Open surgery
Greenberg et al. [32] 2008 372 1 14 22 10 2 Reimplanted or bypassed Yesa None
Conrad et al. [18]e 2008 471 7 24 20 13 2 Reimplanted T9-L1, if patent Yes None
Fehrenbacher et al. [22]f 2010 343 1 4.3 5.4 3.1 0 Reimplantated T8—coeliac axis Not routinely MEP
Coselli et al. [11]g 2007 2286 b
3.3 6.3 2.6 1.4 Reimplanted in 61% In 27% None
Bavaria et al. [50] 2007 94 14h b b b b d
Not consistently None
Zoli et al. [53] 2010 609 2.3 2.5 11.5 3.9 2.2 Total sacrifice In 59% MEP/SSEP
Sundt et al. [30] 2011 99 3i 0 0 0 0 Reimplanted, T9-L1 None None
b
Schepens et al. [54] 2009 571 Overall paraplegia 5.3%, paraparesis 3% Reimplanted, T8-L1 Yes MEP/SSEP
d d d d
Safi et al. [39] 2005 1106 10.7% No reimplant in 61% Yes None
Stone et al. [52] 2006 83 7.2c b b b b d d
Not reported
Perfusion, temperature and the anaesthesiological perioperative management for open repair varied significantly among reference centres, e.g. Sundt et al.: DHCA at 18°C; Schepens et al.: moderate hypothermia at
32°C, DHCA only if proximal clamping is impossible; Zoli et al.: full cardiopulmonary bypass, partial cardiopulmonary bypass, left heart bypass and DHCA.
SCI: spinal cord injury; TEVAR: thoracic endovascular aortic repair; DTA: descending thoracic aorta; CSF: cerebrospinal fluid; MEP: motor evoked potential; SSEP: somatosensory evoked potential; DHCA: deep
hypothermic circulatory arrest.
a
‘At the discretion of the treating physician’.
b
Excluded.
c
DTA patients treated for degenerative pathology excluding ruptures.
d
Not reported.
e
Intraoperative epidural cooling (EC) to 25–27°C until reperfusion of the lower extremities.
f
Singularly operated in DHCA, SA reimplant, no CSF drain (!).
g
Selective perfusion (balloon catheters) to the coeliac and superior mesenteric arteries, renals intermittently with 4°C crystalloid, left heart bypass in 40%, 60% ‘clamp-and-sew’ 32–34°C.
h
The Gore TAG non-randomized multicentre trial: significantly higher incidence of symptomatic aneurysms (38 vs 21%, P = 0.007) in the surgical control group, historically and retrospectively acquired; surgeons
performing the open procedures were from various surgical backgrounds; there was a variable volume of thoracic aortic surgery performed in each contributing centre, and a variable use of spinal cord protection
techniques. For example, in the open repair group 75% of the paraplegic patients died in hospital.
i
Delayed paraplegia secondary to persistent hypotension; the comparison is not representative as patient characteristics are not uniform, e.g. urgent/emergent procedures—see original data for details.
Table 4: Mechanisms of spinal cord ischaemia in open repair and during thoracic endovascular aortic repair (TEVAR)
Insult Effect
Open repair
(Prolonged) aortic cross-clamping Acute loss of direct (SAs) and indirect (collateral network) cord perfusion
REPORT
Decrease in mean arterial pressure (e.g. due to anaesthesia and Insufficient spinal cord perfusion pressure (resulting in acute, generalized malperfusion of
extracorporeal circulation) the cord)
Increase in CSF pressure Counteracts spinal cord perfusion pressure triggering a ‘spinal compartment syndrome’
Loss of critical SAs Acute loss of direct spinal cord perfusion
Insufficient distal perfusion pressure (on pump/no pulsatility) Inadequate distal inflow to the collateral network
Arterial steal phenomenon via patent SAs after opening the Reduced SCPP ! oedema of the spinal cord
aneurysm sac
Reperfusion injury after cross-clamping Spinal cord oedema (beginning a ‘vicious cycle’)
Postoperative thrombosis of the spinal cord-supplying vessels May be responsible for delayed paraplegia (e.g. after TEVAR)

TEVAR
TEVAR covering of left subclavian artery, intercostal and lumbar Reduction in proximal, medial and distal direct and collateral arterial blood flow to the
SAs, hypogastric arteries and sacral arteries spinal cord
Previous distal aortic surgery If the hypogastric axis was compromised/sacrificed, distal collateral inflow is
compromised
Severe peripheral vascular disease Reduction in (predominantly distal) collateral inflow also due to the impairment of flow
provided to the collateral network by the hypogastric arteries
CSF: cerebrospinal fluid; SA: segmental arteries.
Figure 1: Spinal cord blood flow and perfusion pressure during thoracic aortic occlusion. The changes (arrows) represent the response to aortic cross-clamping per se.
: increase; : decrease; ICP: intracranial pressure.
what was thought to be the Artery of Adamkiewicz using magnetic arteries in the spinal canal, perivertebral tissues and paraspinal
resonance angiography [72–75]. muscles that receives input from the subclavian, internal thoracic,
Within the spinal canal, there is an axial network of small arteries lumbar and hypogastric arteries (Figs 2B and C and 3). These small
that connect with each other as well as with major arteries that arteries are connected with each other and with the ASA and PSA
supply the spinal cord [37]. Blood supply to the spinal cord is even providing blood flow to the spinal cord. This network can increase
more complex and pathologically modified in patients with aortic blood flow from one source when another is impaired. Conversely,
diseases. In almost 25% of these patients, most SAs are occluded a steal effect can occur—spinal cord blood flow can be reduced if
and spinal cord integrity is maintained by an extensive collateral an alternative lower resistance pathway becomes patent elsewhere
network in which lumbar arteries and the pelvic circulation are re- in the circulation. The concept of collateral circulation is most prob-
sponsible for main blood supply. Reimplantation of SAs increases ably the reason why the maintenance of high arterial blood pres-
aortic cross-clamp time and possibly aggravates intraoperative sure and cardiac index may reduce SCI in TAAA surgery.
spinal cord hypoperfusion due to blood loss via back bleeding. Reimplantation of significant patent SAs has been associated
Probably, a substantial percentage of reimplanted SAs occlude with decreased rates of SCI [43]. However, if a particular branch is
early. Alternative surgical techniques for reimplantation include small or occluded, a great deal of time may be spent without
latero-lateral aortic patch reimplantation or the use of small-calibre benefit—possibly even causing harm to the spinal cord increasing
(≤5 mm) bypass conduits such as vein grafts or vascular prostheses. the risk of intraoperative SCI. Intercostal reimplantation (IRP) may
The alternative paradigm suggests—in addition to the radicular jeopardize spinal cord blood flow by back bleeding. Even after
arteries—that the spinal cord also has a complex collateral circula- successful revascularization of a dominant SA, symptomatic SCI
tion. It is hypothesized that there is also an axial network of small may be observed. On the contrary, IRP may jeopardize spinal cord
SAs with small catheters after opening the aneurysm is another

Table 5: Strategies to prevent and treat spinal cord ischaemia option (with caution in patients with connective tissue disease) if
an island repair is planned. A novel approach termed ‘minimally
Minimizing spinal cord ischaemic time invasive segmental artery coil embolization’ (MISACE) is an elegant
Multisegmental, sequential reconstruction of the aorta alternative recently introduced as an option allowing for endovas-
Stepwise or staged or sequential clamping of the aneurysm cular staging to precondition spinal cord blood supply, avoiding
(if anatomy permits to do so) ‘steal’ and type II endoleaks and shortening cross-clamp time.
Increasing tolerance to ischaemia
Deliberate utilization of mild systemic hypothermia
Several methods have been used to provide reperfusion on the
Optional deep hypothermic circulatory arrest and/or selective spinal one hand and avoid back bleeding of these arteries on the other
cord hypothermia by epidural cooling hand. One approach is to preserve a fragment of the back wall of
Pharmacological neuroprotection/ischaemic preconditioning the aneurysm where large SAs arise and use it during aortic recon-
(‘staged repair’)
struction with the idea to restore critical perfusion. Another ap-
Augmenting spinal cord perfusion
Deliberate proximal and distal hypertension proach is to attach critical SAs via a second prosthesis into the
Cerebrospinal fluid (CSF) drainage aortic prosthesis. Furthermore, to prevent significant steal via back
Reimplantation of segmental arteries bleeding, non-critical arteries are occluded with surgical clips

Preservation of subclavian artery and hypogastric artery flow/left from outside or oversewn from inside. A common mistake is to
heart bypass/distal aortic perfusion
Early detection of spinal cord ischaemia
aim for reimplantation of the vigorous ‘back bleeders’—but these
IOM (MEP and SSEP) are the arteries that are sufficiently collateralized—rather than
Fast track concept and serial postoperative neurological examination those SAs that do not bleed back. As the time required for reim-
plantion of all SAs potentially increases the risk of SCI, intraopera-
IOM: intraoperative neurophysiological monitoring; MEPs: motor tive neurophysiological monitoring (IOM) may direct the surgeon
evoked potentials; SSEPs: somatosensory evoked potentials. during sequential cross-clamping and provide information about
which vessels are essential for sufficient spinal cord perfusion.
However, the success of this strategy is controversial and the rates
blood flow by back bleeding. By using ligation or clipping of SAs of SCI with this strategy have not proved to be superior.
( preferably prior to opening the aneurysm sac), the blood flow is Because of the key role of pelvic circulation mainly provided by
directed to the spinal cord by collateral vessels and the need for the hypogastric arteries, many patients are critically dependent on
revascularization becomes futile. Therefore, it might be more im- distal (retrograde) perfusion from LHB. Partial LHB provides a con-
portant to consider the superior and inferior supply of the spinal trolled perfusion of the distal aorta by directing blood from the
cord via the subclavian arteries and the internal iliac network left atrium to distal segments. Flow is controlled by a centrifugal
(e.g. the hypogastric arteries). At least unilateral internal iliac artery pump or a complete circuit with a membrane oxygenator accord-
perfusion should be strictly maintained. Careful consideration is ing to the department policy. During partial LHB with a proximal
also warranted in the treatment of common and internal iliac aortic cross-clamp, the distal aortic cross-clamp can be moved
aneurysms particularly in endovascular repair. A branched stent- from proximal to distal as repair of the descending aorta pro-
graft should be used if possible—otherwise primary embolization, gresses to minimize end-organ ischaemia, a technique that has
e.g. with Amplatzer plugs seems to cause (at least) less buttock is- been termed ‘sequential repair’ by Coselli et al. A large amount of
chaemia. However, patients with poor pelvic circulation are critic- retrospective data suggests that the use of LHB in extensive TAAA
ally dependent on the above-mentioned specific ICAs. In these reduces the risk of ischaemic complications. The absence of an
cases, reimplantation of critical SAs (Th8-L4) may be considered. oxygenator in the LHB system necessitates less heparinization,
which is associated with considerable reduction in bleeding.
However, it effectively improves oxygenation during one-lung
STRATEGIES TO SHORTEN THE INTRAOPERATIVE ventilation, especially as these patients frequently are smokers
DURATION OF SPINAL CORD ISCHAEMIA with varying extent of chronic obstructive pulmonary disease
(COPD) [78]. In addition, LHB allows for selective perfusion of
The duration of aortic cross-clamping has a close relationship to mesenteric branch vessels through separate balloon-blocking
the risk of SCI. For this reason, one major objective of surgery is to catheters. Summarizing, LHB facilitates both afterload reduction as
keep the overall ischaemic time short. well as cooling and rewarming, avoids vasodilators, increases distal
Open TAAA repair starts by clamping the proximal and distal aortic pressure for patients dependent on caudal vessels, reduces
aorta to isolate partially (sequential or staged repair) or totally the an increased CSF pressure and decreases the risk of visceral ischae-
diseased segment if the patient is operated on with LHB. Unless mia and spinal cord ischaemia by permitting selective organ and
distal aortic perfusion via extracorporeal circulation support is segmental artery perfusion. However, LHB does not appear to be
initiated, there is no or only minimal blood flow below the cross- the ultimate methodology for all cases: this especially applies to
clamp. Spinal cord perfusion is sustained only via the vertebral, Crawford Type I and II aneurysms, where the rate of SCI is still high.
cervical and subclavian arteries. Thus, spinal cord perfusion pres-
sure (SCPP = radicular artery end pressures minus the greater of
venous or CSF pressures) may be compromised [76, 77]. Important
arteries arising from the aortic aneurysm sac are no longer per- STRATEGIES TO INCREASE SPINAL CORD
fused. In case of back bleeding, the steal phenomenon will add- TOLERANCE TO TRANSIENT ISCHAEMIA
itionally reduce both collateral network pressure and thereby
perfusion pressure of the ASA. Therefore, it is important to avoid The highly metabolic grey substance of the spinal cord is more
back bleeding instantly by oversewing (or preferably prior to aneur- sensitive to ischaemia than the white substance. Under nor-
ysm sac opening by clip occlusion); blocking of the corresponding mothermic conditions, the central nervous system poorly tolerates
REPORT
Figure 2: (A) Blood supply to the spinal cord. Schematic drawing of the spinal cord with indications of areas supplied by the posterior and the anterior spinal arteries.
Radicular arteries are variable in location. The inflow to spinal arteries is divided into three main supply zones ASA: anterior spinal artery; PSA: posterior spinal artery;
PICA: posterior inferior cerebellar artery; SA: segmental arteries; ICA: intercostal arteries; LA: lumbar arteries. (B) Anatomy of the collateral network from experimental
casts, sagittal (B0 1) and dorsal (B0 2) views. Macroscopic appearance of the pair of dorsal segmental vessels at L1. The dorsal process is removed. In B0 1, the X designates
the paraspinous muscular vasculature providing extensive longitudinal arterioarteriolar connections in B0 1 and B0 2; the triangle indicates iliopsoas muscle; the double
arrow indicates anterior spinal artery [reprinted from Etz et al. [37] Copyright (2011) with permission from Elsevier]. (C) Relationship of the ASA and the repetitive epi-
dural arcades in a Yorkshire pig model. V indicates the epidural venous plexus. Anterior to the extensive venous plexus, four arteriolar branches (yellow arrows) con-
tribute to one circular epidural arcade. This pattern is repeated at the level of each vertebral segment. These vascular structures connect segments side to side as well
as longitudinally. Green arrows depict the anterior radiculomedullary artery, which connects directly with the anterior spinal artery [reprinted from Etz et al. [37]
Copyright (2011) with permission from Elsevier].
ischaemia, manifesting neuronal dysfunction and injury within Additionally, delayed postoperative rewarming might have a positive
5 min after the cessation of blood flow. When incomplete ischae- effect on ischaemia tolerance of the spinal cord and therefore is part
mia is produced, SCI generally does not occur with an aortic of the postoperative protocol at some institutions. However, there is
cross-clamping time of less than 15 min. As the cross-clamp time not yet enough clinical evidence or prospective randomized studies to
is prolonged, the risk of SCI gradually increases. It is important to proof this concept.
note that the risk of SCI is closely related to the body core tem- The protective effect of hypothermia is thought to be primarily
perature during lower body circulatory arrest, initiated by placing a consequence of the decreased metabolic demands associated
the cross-clamp: Kamiya et al. [79] found a 6-fold increase in the with reduced spinal cord oxygen consumption. However, hypo-
incidence of SCI in their subgroup analysis of patients undergoing thermia may also protect the cell by stabilizing membranes and
prolonged distal circulatory arrest at only moderate hypothermia. attenuating the inflammatory and excitotoxic responses to ischae-
Experimentally, the safe period of distal arrest has been shown to be mia during reperfusion. Further protection of the spinal cord
widely overestimated and irreversible SCI at 28°C occurs earlier than tissue has been attempted with regional spinal cord hypothermia
expected [80]. The only intervention in humans that has consistently (epidural cooling) [70]. However, besides contamination issues, re-
proved to be effective in protecting the central nervous system from sponsive hyperperfusion and consecutive development of oedema
ischaemia during the absence of blood flow is hypothermia [81–83]. are feared by some after cooling is ended.

Figure 3: A schematic diagram of the blood supply to the spinal cord demonstrates the relationships, relative sizes and the interconnections among the segmental
arteries (SAs), the anterior radiculomedullary arteries (ARMAs), the epidural arcades and the anterior spinal artery (ASA). The longitudinal anastomoses along the
dorsal processes of the spine as well as dorsal communications (interstitial connections) between the right and the left branches of segmental arteries are also shown
[reprinted from Etz et al. [37] Copyright (2011) with permission from Elsevier].
In addition to lowering oxygen consumption, the risk of intra- cross-clamp, depending on distal aortic perfusion via LHB or
operative spinal cord ischaemia may be avoided or minimized by extracorporeal circulation with an oxygenator and (iii) from the
improving oxygen delivery via an increase of SCPP. Demand side central venous and CSF pressure. During proximal aortic cross-
interventions prolong ischaemic tolerance by decreasing the need clamping, the MAP inceases considerably and needs pharmaco-
of oxygen (barbiturates and hypothermia), while reducing the logical correction to control left ventricular afterload. The elevated
levels of neurotoxins released during ischaemia and/or their dele- cerebral blood pressure during proximal aortic cross-clamping
terious effects (naloxone and hypothermia). The spinal cord may may result in an overproduction of CSF and an elevation of CSF
be directly protected against neuronal injury at the cellular level pressure. Elevated CSF pressure further reduces the SCPP. If CSF
by reducing hyperaemic and inflammatory responses (hypother- pressure exceeds both ASA and PSA pressure, the spinal cord
mia, steroids and free radical scavengers). Supply side interven- blood flow ceases and oxygen supply is interrupted—the spinal
tions increase spinal cord blood supply and tissue oxygen delivery cord is suffering ischaemia. Full or partial recovery from delayed
by maximizing collateral blood flow to the spinal cord, reducing postoperative SCI after open or endovascular repair has been
spinal fluid pressure, increasing arterial blood pressure and the reported and emphasizes the effectiveness of acute interventions
cardiac index during and after the repair, preventing steal and to improve spinal cord perfusion, if applied instantly. Postoperative
guaranteeing sufficient oxygenation during aortic cross-clamping. events such as hypotension due, for instance, to haemorrhage or
The observation that similar reductions in SCI can be achieved by increased CSF pressure may also increase the risk of SCI after open
combining different therapies basically reflects the complexity of and endovascular repair. Therefore, maintaining adequate spinal
spinal cord blood supply and neuronal injury. cord perfusion by increasing arterial pressure and augmenting
cardiac output, together with preventing hypotension, lowering CSF
pressure and reducing central venous pressure (CVP), is important
for the prevention of spinal cord ischaemia.
STRATEGIES TO AUGMENT SPINAL CORD CSF production rises during ischaemia, causing an increased CSF
PERFUSION pressure soon after cross-clamping. To minimize spinal cord ischae-
mia, CSF drainage is used to maintain a low CSF pressure while im-
As previously elaborated on, spinal cord perfusion during aortic proving net perfusion pressure. The physiological basis for lumbar
surgery depends on (i) the ASA flow from radicular vessels arising CSF drainage is given by the SCPP being a direct function of the
above the proximal cross-clamp and supplied by proximal aortic MAP minus lumbar CSF pressure (or alternatively central venous
pressure, (ii) from vessels arising from the aorta below the distal pressure). Therefore, an increased CSF pressure decreases the
SCPP. Draining CSF has the potential to increase the SCPP by in blood pressure during and early after the procedure. Equally, an
decreasing the CSF pressure. Experiences during open surgical intensive care unit that is familiar with all aspects of postoperative
DTA/TAAA repair have shown that this intervention has a positive care after TAA/A repair is very important to provide maximal
effect on neurological outcome. In general, introduction of a CSF haemodynamic stability. Many patients with late onset SCI have a
catheter is performed preoperatively, but can also be performed documented period of instability prior to symptoms.
postoperatively when neurological symptoms develop. It is highly Spinal cord perfusion can be surgically augmented by reattach-
REPORT
advisable to insert a CSF drain in all patients undergoing TAA/A ment of SAs into the vascular graft if the surgeon respects the ana-
surgery or thoracoabdominal EVAR and measure CSF pressure for tomical paradigm that direct segmental blood flow is the most
at least 48 h postoperatively. If CSF pressure was allowed to rise important intervention to reduce the risk of SCI. Large SAs with
postoperatively in combination with a period of blood pressure little or no back bleeding may be particularly important for spinal
instability, late onset SCI due to spinal cord oedema may occur. cord perfusion. Alternatively, occlusion or oversewing of strong
CSF should be drained into a sealed reservoir to achieve a CSF back bleeding SAs has been advocated to improve spinal cord
pressure of 10 mmHg; some institutions alternatively aim for the perfusion by preventing an arterial steal effect and shortening
preoperative ‘opening pressure’ immediately after CSF catheter intraoperative ischaemic time [3]. As most reports combine IRP
placement as an individual baseline pressure of the patient. CSF with other strategies, it is hard to determine how much reattach-

drainage appears to be a safe method even in patients subjected ment of SAs contributes on its own to improved results, even
to full anticoagulation for extracorporeal circulation. Complica- though it is frequently presented as the factor primarily respon-
tions associated with this technique occur in up to 1% of patients sible for reducing SCI.
and include intracranial hypotension, subdural haematoma, On the other side, a significant reduction in the risk of SCI
intracranial haemorrhage, remote cerebellar haemorrhage, spinal without IRP was obtained by increasing ischaemic tolerance and
headache, persistent CSF leak, intraspinal haematoma, catheter maximizing collateral circulation to the spinal cord. Significantly,
fracture, meningitis and direct SCI. Some institutions insert the this technique maintains high proximal arterial blood pressure
CSF catheter on the evening prior to surgery to avoid or anticipate during aortic occlusion. These findings show that spinal cord in-
bleeding complications. The most serious complications appear farction can almost always be prevented without any IRP if ischae-
to be associated with intracranial hypotension from rapid or too mic protection and collateral circulation to the spinal cord are
much CSF drainage. Precautions, such as continuous measurement sufficient [3]. Although this approach considerably reduced imme-
of CSF pressure, controlled intermittent CSF drainage and assess- diate SCI, delayed SCI still occurred in a few patients days to weeks
ment of coagulation function, decrease the risks associated with CSF after surgery [29]. The occurrence of delayed SCI shows the limita-
drainage. tions of perioperative ischaemic protection and of the mainten-
Augmentation of the MAP (in combination with CSF drainage if ance of collateral circulation strategies to prevent infarction [29].
not already present) is another technique for the treatment of Recent advances in magnetic resonance angiography have per-
spinal cord ischaemia. In general, vasopressor agents such as nor- mitted a more precise imaging of the ASA and the expected most
epinephrine are administered to maintain an MAP of 80–100 important SAs in patients with TAAA. It provides a method to ana-
mmHg to ensure an SCPP of at least 70 mmHg. A more recent tomically identify SAs for potential reimplantation. Non-selective
clinical study suggested that failure to maintain a patient’s individ- IRP may also be protective by additionally increasing perfusion
ual preoperative arterial baseline pressure during the early post- pressure in the collateral circulation and feeding the greater ra-
operative period after TAA/A repair is strongly associated with dicular artery. This suggests that any SA can supply blood to the
delayed postoperative SCI [29]. The MAP can be further increased spinal cord and may evolve into collateral circulation to the ASA.
in 5 mmHg steps in case of persisting SCI. When arterial pressure In patients with reduced collateral circulation, reimplanting any
increases, it is also important to assure a satisfying cardiac output SA in the critical zone of T8 to L1 may permanently increase per-
and to guarantee an optimal oxygen delivery (control of haemoglo- fusion pressure in the collateral network. This may be the import-
bin). Inconsistent arterial pressure control may also partly explain ant factor to avoid spinal cord infarction, regardless of whether
the controversy surrounding the effectiveness of CSF drainage as specific identified intercostals are reimplanted.
an exclusive means to decrease CSF pressure. Hypotension from Techniques that rely on extensive IRP based on changes in
bleeding or other causes is often associated with the onset of SCI evoked potentials (EPs) may be successful not because SAs identi-
after TAAA repair. Nevertheless, clinical observations suggest that fied by ischaemic changes were reimplanted, but because reim-
SCI may as well contribute to hypotension due to generalized planting so many SAs increased the perfusion pressure in the
vasoplegia. In some patients, spinal cord ischaemia-associated collateral circulation. By reimplanting SAs as an aortic button
hypotension is caused by neurogenic shock with autonomic dys- using a side clamp after the distal anastomosis is completed, it is
function. In this situation, hypotension may not be the cause but possible to achieve high SA patency without significantly increas-
represent an early sign of SCI and the beginning of a vicious cycle. ing aortic occlusion times. These findings suggest that factors
An immediate treatment of hypotension associated with spinal related to spinal cord ischaemia as well as collateral circulation
cord ischaemia is necessary to prevent permanent SCI. Finally, ar- account for most of the SCI risk in TAAA surgery and that IRP, al-
terial pressure should be monitored carefully when antihyperten- though not necessary to prevent SCI in most patients, is critically
sive therapy is resumed after successful open or endovascular important in a few. Since we do not yet know how to identify the
TAA/A repair to avoid unintentional hypotension. Nitroprusside very patients who will sustain SCI without IRP, it is important to
derivatives should be strictly avoided due to possible arterio- reimplant SAs only without substantially increasing intraoperative
venous shunting. The benefits of postoperative arterial pressure spinal cord ischaemic time and surgical morbidity, even in those
increase must be weighed against the risk of bleeding and the who would not sustain SCI without IRP in order to maximize the
risks associated with temporary arterial pressure elevation. Anaes- benefit for the ones at risk.
thetic staff needs to be well trained in the management of TAAA In TEVAR, it is not possible to preserve blood flow in SAs. If the
surgery and the postoperative patient to prevent large variations left subclavian artery requires coverage by the stent-graft to
enable complete exclusion of the aneurysm or to allow for a spinal cord may cause a selective motor deficit with intact sensa-
better proximal landing zone, subclavian arterial flow should be tion. In this situation, SSEP monitoring may fail to detect spinal
preserved by prior transposition of the subclavian artery onto the cord ischaemia. This anatomical picture is likely an oversimplifica-
left common carotid artery. Another approach to preserve left tion, because SSEPs from the lower extremity are thought to
subclavian artery flow in TEVAR is to perform a left carotid to sub- include a contribution from the spinocerebellar pathways that are
clavian bypass graft with ligation or coil embolization of the prox- located deeper in the spinal cord. Since the latter contribution is
imal left subclavian artery stump. Maintaining blood flow in the vascularized by the ASA, it is possible that the SSEP may respond
left subclavian artery is important for spinal cord perfusion as its to selective anterior ischaemia by the effect on this component of
branches supply the ASA. Meanwhile, there is substantial evidence the pathway. Alternatively, anterior ischaemia may steal blood
available supporting routine preservation of the left subclavian from the posterior perfusion, leading to SSEP changes. As SSEPs
artery [84, 85]. are primarily a white substance pathway in the spinal cord and
largely devoid of synaptic connections, they may react less sensi-
tively than MEP pathways that include synapses. However, SSEPs
recorded in the spinal cord are known to be sensitive to hypoten-
STRATEGIES TO DETECT SPINAL CORD sion and have been used to gauge deliberate hypotension during

ISCHAEMIA TAAA surgery. The sensitivity of SSEPs to distal perfusion has
resulted in substantial false-positive changes. As aortic cross-
Early detection of spinal cord ischaemia is important as it permits clamping compromises perfusion of the anterior spinal cord and
early intervention before ischaemia evolves to infarction. SSEPs results primarily in motor deficits, it is not surprising that SSEP
and MEPs are established methods of spinal cord monitoring monitoring during TAAA surgery with distal aortic perfusion has
during TAAA surgery and TEVAR. The clinical objectives for SSEP/ not reduced the incidence of neurological deficits.
MEP monitoring are to ensure adequate spinal cord perfusion Monitoring of motor pathways, particularly in case the function
throughout the procedure, to identify critical vessels for reimplan- of alpha motor neurons is included, is a sensitive measure of an-
tation and to establish an MAP adequate for spinal cord perfusion. terior spinal cord function. To ensure that only motor pathways
Decreased EP amplitudes have proved to correlate with spinal are stimulated, electrical or magnetic stimulation of the cerebral
cord ischaemia, but the sensitivity and specificity of these techni- cortex is used to produce descending volleys of activity in the cor-
ques for detection of spinal cord ischaemia remain to be deter- ticospinal tracts. Following the pathway of motor function, MEPs
mined. Intraoperative changes or loss of EP signals are not always elicited through transcortical electrical stimulation appear to be a
caused by spinal cord ischaemia. A functioning peripheral nerve is more specific monitor (Fig. 4). Transmission may be evaluated by
required to generate both SSEP and MEP signals. Therefore, per- recording from the distal spinal cord using epidural recordings
ipheral nerve ischaemia from any cause will affect the associated (evoked spinal cord volley, epi-MEP), from a peripheral nerve
SSEP or MEP amplitudes. Vascular malperfusion of a lower ex- (neurogram) or from muscles (compound muscle action poten-
tremity can cause a loss of peripheral EP in the absence of spinal tials,). Unfortunately, epi-MEPs are less sensitive to the degree of
cord ischaemia if blood flow to the limb is significantly impaired. spinal cord ischaemia because they do not involve the anterior
Lower extremity malperfusion may be caused by aortic dissection horn cell and their axons are less sensitive to ischaemia than grey
itself, atheroembolism or most commonly by arterial cannulation matter.
of the femoral artery for extracorporeal circulation. Similar to mal- MEP monitoring has been used to identify SAs critical for re-
perfusion, aortic cross-clamping without distal aortic perfusion attachment following the acute loss of lower extremity MEP
results over time in fading EP signals from the lower extremities. signals during TAAA repair. MEP recording during surgery may
Acute intraoperative stroke may also produce EP changes. They guide the physician in determining the optimum postoperative
can be distinguished from changes caused by spinal cord ischae- blood pressure. In patients with a significant risk of spinal cord is-
mia by comparing signals recorded at different sites along the chaemia, sequential cross-clamping of the aorta may identify the
neural conduction pathway. Stroke is associated with selective loss critical segments of the aorta that provide important blood
of cortical signals and typically affects the EP from both upper and supply to the spinal cord. MEPs may therefore be used to guide
lower extremities. the need and level of intercostal and lumbar SA reattachement.
SSEP recordings measured via the sensory cortex can be Although this method of monitoring spinal cord function may be
affected by ischaemia of the peripheral nerves, the spinal cord, useful in studying the effectiveness of adjuncts to lower the risk
the brainstem, the sensory cortex and additionally by technical of SCI, it sometimes provides false-positive results; particularly
and anaesthesiological factors (Fig. 4). An advantage of SSEP mon- since the neurological function of the spinal cord may be
itoring is that it is relatively safe to perform and easy to interpret affected by anaesthetic agents that potentially depress the syn-
by comparing the amplitude and latency of SSEPs recorded from aptic function of the cerebral cortex and spinal grey substance.
the upper and lower extremities. The fidelity of SSEPs is improved In particular, the amplitude of the MEP is sensitive to neuromus-
with neuromuscular blockade under general anaesthesia. Although cular blocking agents and many general anaesthetic agents.
high concentrations of inhaled anaesthetics, thiopental or propo- General anaesthetic regimens utilizing intravenous infusions of
fol can attenuate cortical SSEP signals, a balanced general and remifentanil, ketamine, propofol or etomidate without neuro-
inhaled anaesthetic provides consistent conditions for intraopera- muscular blockade or carefully controlled incomplete neuro-
tive SSEP monitoring. Anatomically, the SSEP travels cephalad via muscular blockade are often required to maintain satisfactory
the peripheral nerve and enters the dorsal roots of the spinal cord MEP signals during operation.
corresponding to the stimulated nerve. It traverses the dorsal horn Recently, near-infrared spectroscopy has been successfully
and ascends the spinal cord via the dorsal spinal cord that med- introduced into a clinical pilot study to non-invasively detect
iates proprioception and vibration. A potential limitation of SSEP spinal cord ischaemia during open thoracic/thoracoabdominal
monitoring is that spinal cord ischaemia confined to the anterior repair. Sensitivity and response time are promising, but further
REPORT
Figure 4: Left upper panel: physiological somatosensory evoked potentials (SSEPs). Right upper panel: pathophysiological SSEPs. Left lower panel: physiological motor
evoked potentials (MEPs). Right lower panel: pathophysiological MEPs.
research has to validate this method experimentally and clinically to of large-bore sheaths placed in the iliac arteries during the proced-
define its role in relation to IOM to detect spinal cord ischaemia [86]. ure) and negative effects on spinal cord perfusion associated with
Finally, another eventual limitation used as an argument by open TAAA surgery. Distal aortic perfusion remains uninterrupted,
some is that the method of IOM is complex and renders the pro- guaranteeing a continuous blood flow to the spinal cord and ex-
cedure even more cumbersome due to the equipment required cluding a steal effect via SAs after opening the aneurysm. Delayed
in the operation theatre and the contribution of a neurophysiolo- paraplegia may occur due to (micro) embolism caused by athero-
gist during the entire procedure [87]. Not all institutions are able sclerotic debris or blood clots flushed into the spinal cord vascula-
to provide such an environment. ture after being mobilized from the aneurysm sac during partial
and/or temporary perfusion which may occur in type II endoleaks.
Reperfusion injury after open surgical aortic replacement can
TEVAR—SPECIAL CONSIDERATIONS occur when cytotoxic metabolites formed during cross-clamping
reach the reimplanted SAs. Considering avoidance of SCI after
TEVAR has made us rethink the pathophysiology of spinal cord is- TEVAR, it must be remembered that the extent of repair is of im-
chaemia. Coverage of the thoracic aorta without revascularization portance to determine the risk of SCI. The reduced risk of SCI in
of SAs feeding the spinal cord was expected to produce higher TEVAR compared with open TAAA surgery is multifactorial. If a
rates of spinal cord ischaemia than actually observed. TEVAR may series contain patients with a shorter length of covered aorta, they
be performed with CSF drainage. Other adjuncts believed to be will inevitably show lower rates of spinal cord ischaemia. Likewise,
necessary in avoiding spinal ischaemia such as revascularization of when a dissected aorta is stented, retrograde perfusion of the false
important intercostal branches cannot be employed and, still, the lumen via communications in the membrane maintains SA blood
rates of SCI are low thereby supporting the collateral network supply. This is clearly not a phenomenon that occurs after surgical
concept (and the strategy of SA sacrifice in open TAA/A repair). repair and complete exclusion of the lesion.
TEVAR has less influence on the patient’s perfusion physiology, However, the issue of SCI still remains with TEVAR because of (i)
ensures cardiovascular stability and offers shorter or no organ is- the inability to revascularize covered SAs, (ii) a period of hypoten-
chaemic periods as aortic cross-clamping is not necessary during sion for TEVAR deployment, (iii) the persistence of the risk of em-
TEVAR, thereby avoiding distal hypotension (except for the duration bolization from aortic atheromatous lesions and (iv) the possibility
of compromise of distal perfusion due to large-bore sheaths used Dong et al. reported a 5.4% SCI rate in a series of 56 TAA/A opera-
for stent-graft introduction during the procedure. Consequently, tions utilizing MEP and SSEP monitoring with a reimplantation ap-
SCI remains the most devastating complication also after TEVAR. proach. The majority of studies that sought to prevent ischaemia
Independent proven risk factors for the development of delayed- by reimplantating SAs with particular focus on the area between
onset SCI are (i) perioperative MAP of less than 70 mmHg, (ii) CSF T7 and L2 anticipated that SCI is the consequence of hypoperfu-
drainage complications, (iii) previous abdominal aortic aneurysm sion after sacrifice [10, 69]. Several studies have attempted to dem-
repair (if the hypogastric arteries have been compromised), (iv) sig- onstrate the arguable superiority of this approach. In contrast, in
nificant preoperative renal insufficiency, (v) left subclavian artery 1994 and 1996, SCI rates as low as 3% in DTA/TAAA repair without
coverage without revascularization and (vi) the use of three or more SA reimplantation were described both in a series of 110 by Acher
stent-grafts (reflecting the lengths of the covered segments as well as et al. [97], and in 95 consecutive patients by Griepp et al. [ 99].
the lengths of the procedural time). However, others have shown In 2004, Ohtsubo et al. proposed the selective perfusion of the
that the impact of simultaneous closure of two independent arterial Artery of Adamkiewicz to prevent intraoperative spinal cord is-
spinal-cord supplying vascular territories (in particular in combin- chaemia [100]. Furukawa et al. in their most recent contribution
ation with intraoperative hypotension) is the most important risk proposed a sophisticated, integrated intraoperative approach: se-
factor for symptomatic SCI irrespective of the covered length or pre- lective intraoperative perfusion of the identified artery to prevent

vious aortic repair, underscoring the importance of the collateral ischaemia during aortic cross-clamping, temporary clamping of
network concept [88]. A thorough consideration of the risk profile in SAs during aortic cross-clamping to prevent steal once the aneur-
patients requiring TEVAR remains essential. Careful haemodynamic ysm sac is opened (along with neuroprotective adjuncts like CSF
monitoring is vital and prophylactic measures for spinal cord protec- drainage and high MAP) and reconstruction of those SAs deemed
tion should be considered in patients whose thoracic aortas require relevant for the supply of the Artery of Adamkiewicz to restore
extensive coverage and those with other independent risk factors. native spinal cord perfusion [100]. Although only a very small
When TEVAR is performed in patients with chronic atheroscler- series, 44% of the reconstructed SAs were occluded in the post-
otic aneurysm in contrast to the ones with acute aortic dissection, operative follow-up, and the only case of SCI occurred in the
collaterals may have developed with time and are able to com- group with SA reconstruction [101]. Acher, a former proponent of
pensate for acute SA occlusion. Many studies have underlined the SA sacrifice who had switched to a very sophisticated reimplanta-
importance of these individual collateral arterial networks supply- tion strategy in 2005 using preoperative magnetic resonance
ing the spinal cord in patients undergoing TEVAR. Neurophysio- angiographic localization to identify the Artery of Adamkiewicz,
logical monitoring is viewed as an effective method to detect has stated recently (in December 2010) that ‘it remains unclear
spinal cord ischaemia during these procedures [89]. In patients whether intercostal reimplantation reduces paraplegia risk, as we
with deteriorating SSEPs or MEPs, a decrease in the SCPP and/or had initially proposed’ [43, 97].
the CVP as well as an increase in the MAP is obligatory to ensure SCI remains a multifactorial problem with several aetiologies,
sufficient collateral spinal cord perfusion. contributing factors and underlying aortic pathologies and may vary
Recently, an approach to enhance collateralization has been considerably among different patient cohorts. No single spinal
reported as minimally invasive selective segmental artery coil cord protecting method is currently able to provide absolute safety.
embolization before TEVAR or open repair (MISACE) [90]. The Included is SCI as a consequence of the underlying pathology,
method seems to be effective but extensive clinical work has to be ischaemic injuries from loss of distal aortic perfusion, ischaemic in-
done before a recommendation can be made. juries from loss of critical intercostal and lumbar SAs during the
procedure, and other perioperative factors such as hypotension
resulting in delayed SCI. Advanced contemporary surgical and an-
SUMMARY aesthetic methods include reduction of aortic cross-clamp times,
retrograde perfusion via partial LHB, hypothermia, reattachment of
In essence, the surgical community is divided by their respective SAs, CSF drainage, MAP augmentation and IOM, and have improved
hypotheses as to the cause of SCI after TAA/A repair. Those who the safety of thoracic and TAAA repair and TEVAR.
are convinced that SCI is the consequence of chronic hypoperfu- The objective is to rapidly identify the ischaemic condition
sion after sacrifice of SAs critical to spinal cord blood supply do and restore spinal cord perfusion with an attempt to minimize
reimplant SAs, trading prolonged intraoperative spinal cord is- the duration of spinal cord ischaemia. However, even the com-
chaemia for the achievement of arguably superior postoperative bination of these various techniques does not entirely abolish
perfusion [10, 69, 91–96]. Others are convinced that the blood the problem. The practice of coverage of the thoracic aorta by
supply to the spinal cord depends on a highly variable collateral TEVAR and the exclusion of potentially relevant SAs with relative-
system capable of perpetuating sufficient spinal cord perfusion ly low rates of SCI suggest that an exclusively anatomical basis
even after radical sacrifice of (almost all) SAs under stable haemo- concerning spinal cord ischaemia is not a realistic scenario, and
dynamic conditions; this encourages them to omit reimplantation, that the actual individual functionality of the patient’s collateral
shortening intraoperative spinal cord ischaemia by cutting down network, anaesthetic stability and duration of ischaemia seem to
aortic cross-clamp time [3, 97]. play a major role. Despite all these advances and an improved
Reimplantation remains the most widespread strategy for pre- understanding of spinal cord perfusion, spinal cord ischaemia
serving spinal cord function. In 2000, Jacobs et al. [98] reported a and infarction causing postoperative SCI remains an important
significant reduction in neurological complications—to 2.3%—with and debilitating complication of all thoracic and thoracoabdom-
the monitoring of MEPs in a series of 170 patients with TAAA, inal aortic procedures, be it open or endovascular. Associated
using a reimplantation approach with LHB and CSF drainage. van morbidity and mortality justify the routine clinical application of
Dongen et al. [91] reported a 4.2% rate of postoperative paraplegia techniques to prevent and treat SCI. It would be more than
in a series of 118 patients, using hypothermia, LHB and a reim- welcome to gain evidence by randomized controlled trials to
plantation strategy guided by MEP and SSEP monitoring. In 2002, eventually develop widely acceptable algorithms to prevent this
most devastating individual tragedy and significant healthcare realized and formulated. Future research will further provide us
issue. with knowledge on the aetiology, prevention, detection and treat-
Clinical experience supports the efficacy of MAP augmentation ment of SCI.
and CSF drainage for the treatment of delayed-onset SCI caused
by spinal cord ischaemia when applied immediately after appear- Conflict of interest: none declared.
ance of neurological symptoms in patients undergoing open
REPORT
TAAA repair or TEVAR. With regard to intraoperative monitoring:
is EP monitoring mandatory in thoracic and TAAA surgery? The
REFERENCES
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European Journal of Cardio-Thoracic Surgery 47 (2015) 943–957 POSITION STATEMENT

Contemporary spinal cord protection during thoracic and

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C.D. Etz et al. / European Journal of Cardio-Thoracic Surgery

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CSF: cerebrospinal fluid; SA: segmental arteries.

SAs with small catheters after opening the aneurysm is another

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