Next Article in Journal
Association of Physical Activity and Exercise with Physical Performance and Muscle Mass in Older Adults: Results from the Longevity Check-Up (Lookup) 7+ Project
Previous Article in Journal
Comparing Non-Invasive Spectrophotometry to Hematology Analysis for Hemoglobin Measurements in Sickle Cell Disease Patients
Previous Article in Special Issue
Comparison of Immediate, Medium, and Long-Term Postoperative Results of Open Surgery and Fenestrated/Branched Stent Grafts for Extended Thoracoabdominal Aortic Aneurysms
 
 
Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
Journals
JCM
Volume 12
Issue 24
10.3390/jcm12247520
jcm-logo
Submit to this Journal Review for this Journal Propose a Special Issue
► Article Menu

Article Menu

share Share announcement Help format_quote Cite question_answer Discuss in SciProfiles thumb_up
...
Endorse textsms
...
Comment
first_page
settings
Order Article Reprints
Font Type:
Arial Georgia Verdana
Font Size:
Aa Aa Aa
Line Spacing:
Column Width:
Background:
Review

Risk Factors for Spinal Cord Injury during Endovascular Repair of Thoracoabdominal Aneurysm: Review of the Literature and Proposal of a Prognostic Score

by
Laurent Brisard
1,
Salma El Batti
2,
Ottavia Borghese
3 and
Blandine Maurel
3,4,*
1
Department of Anesthesiology and Critical Care, Laënnec Hospital, University Hospital of Nantes, F-44000 Nantes, France
2
Department of Vascular and Endovascular Surgery, Hôpital Européen Georges Pompidou—Hôpitaux de Paris, Université de Paris Cité, F-75015 Paris, France
3
Department of Cardiac and Vascular Surgery, L’Institut du Thorax, Nantes University Hospital, F-44093 Nantes, France
4
Inserm UMR 1087/CNRS UMR 6291, L’Institut du Thorax, Université de Nantes, F-44000 Nantes, France
*
Author to whom correspondence should be addressed.
J. Clin. Med. 2023, 12(24), 7520; https://doi.org/10.3390/jcm12247520
Submission received: 12 July 2023 / Revised: 29 November 2023 / Accepted: 30 November 2023 / Published: 5 December 2023
(This article belongs to the Special Issue Open and Endovascular Management of Complex Aortic Aneurysms)
Browse Figures
Versions Notes

Abstract

:
Despite recent improvements, spinal cord ischemia remains the most feared and dramatic complication following extensive aortic repair. Although endovascular procedures are associated with a lower risk compared with open procedures, this risk is still significant and must be considered. A combined medical and surgical approach may help to optimize the tolerance of the spinal cord to ischemia. The aim of this review is to describe the underlying mechanism involved in spinal cord injury during extensive endovascular aortic repair, to describe the different techniques used to improve spinal cord tolerance to ischemia—including the prophylactic or curative use of spinal drainage—and to propose our algorithm for spinal cord protection and the rational use of spinal drainage.

1. Introduction

The estimated worldwide incidence of spinal cord injuries is between 40 and 80 new cases per million inhabitants per year. This means that between 250,000 and 500,000 people suffer a spinal cord injury every year [1]. Traumatic spinal cord injury is still the most common type of mechanism. Nontraumatic causes are dominated by the ischemic mechanism, which is mainly related to diseases of the aorta. Spinal cord ischemia (SCI) in aortic repair is an old topic of investigation and discussion, first mentioned by Stenonis and Swammerdam in 1667. As early as 1956, Herbert D. Adams emphasized in an essay that the spinal cord is the only organ in which the effects of aortic occlusion are unexplained and that the exact mechanism is unknown [2].
The treatment of complex thoracoabdominal aneurysms has undergone a minimally invasive revolution in the last 20 years. Endovascular repair is now the method of choice for the majority of extensive and complex aortic aneurysms that require extensive incisions and prolonged aortic clamping, as opposed to open repair, which is associated with significant morbimortality.
However, the further development of these complex endovascular techniques is only foreseeable if the adverse events are under control. SCI remains the most feared complication by patients and physicians, as this adverse event completely reverses the benefits of preventive treatment due to its catastrophic consequences: physical and psychological consequences, health costs, and severe disability. In addition, it has a significant impact on the long-term mortality of patients, especially those with permanent damage. The most recent analysis of 1681 patients showed a 1-year survival rate of 90.8% in patients who did not develop SCI versus 73.9% in patients who developed SCI (84.8% in those who developed paraparesis and 66.2% in those who developed permanent deficits) [3]. Regardless of the type of SCI (i.e., temporary or permanent), patients who underwent SCI after TEVAR had a significantly lower 1-year survival rate than patients who did not undergo SCI (65% vs. 87%) [4]. Permanent SCI was associated with a worse 1-year survival rate than transient SCI (54% vs. 80%).
Although endovascular repair has reduced the risk of SCI compared with the open strategy, this risk is still high, ranging from 4% to 50% in the literature [5,6] and 14% in large recent multicenter studies [7]. The SCI rate is lower in high-volume centers and appears to be decreasing in recent years following the use of rigorous multimodality spinal cord preservation strategies [8]. The explanations for this lower rate compared with open surgery are multiple: no aortic clamping, better hemodynamic stability, lower incidence of anemia, faster awakening and recovery.
The mechanisms of occurrence, the risk factors, and the various medical and surgical strategies to prevent SCI need to be fully understood and applied by a multidisciplinary aortic team offering extensive aortic repair. Risk assessment for SCI is a key component for prevention to apply a range of additional preventive medical and surgical measures that are not limited to cerebrospinal fluid drains (CSFDs).
This manuscript reports a preventive multimodal approach to prevent SCI in extensive endovascular repair as described in the literature and applied in our center.

2. Pathogenesis of SCI after Extensive Aortic Endovascular Repair

The blood supply to the spinal cord appears to be more complex than the blood supply to any other system [9,10]. The spinal cord is supplied with blood by an extensive vascular network that extends into the paraspinous muscles and is connected to the subclavian, hypogastric, and internal thoracic arteries [11]. The intercostal and the lumbar arteries give off branches to the spinal arteries, namely the radiculomedullary arteries, which are connected by longitudinal branches and form a dense collateral network. Finally, there is an anterior spinal artery (ASA) and two posterior spinal arteries (PSAs) that run longitudinally along the spinal cord and originate from the vertebral arteries (Figure 1). The largest of the radiculomedullary arteries, the artery of Adamkiewicz, arises most commonly between T9 and T12 on the left and is also a major branch of the ASA [12]. Although in the past it was considered the main vessel supplying the spinal cord, this has been largely questioned, especially since the development of the endovascular era. Several attempts to preserve direct flow into the artery of Adamkiewicz have failed to demonstrate significant benefit.
Thoracic endovascular aortic repair (TEVAR) permanently excludes many of the segmental arteries that are occluded by the covered stent, which may have longer-lasting effects on blood flow in the spinal cord. Remodeling of the collateral network is thought to play an important role in maintaining blood flow in the spinal cord by altering the distribution of blood flow in the intraspinal and paraspinal network after exclusion of the segmental arteries. The restoration of blood flow from the paraspinous to the intraspinous network helps to maintain the viability and function of the spinal cord.
If these compensatory mechanisms are not sufficient or if there is extensive occlusion (due to thrombus formation or embolism) in the intraspinal or paraspinal network, SCI may occur (Figure 2). The occurrence and severity of damage after TEVAR depends on the ability of the collateral network to supply the marginally vascularized area in the spinal cord.
Finally, an important factor that can lead to or exacerbate SCI is embolism and thrombosis of supply branches (Figure 3). This appears to be particularly the case in endovascular interventions, where manipulation of the guidewires in the diseased aorta and placement of stents can lead to dislocation of microemboli in the radiculomedullary arteries [13].
In this context, the maximum symptoms of SCI occur in most patients within 12 to 72 h [14].

3. Risk Factors for Paraplegia

The pathogenesis leading to SCI is complex and multifactorial. Numerous reports have documented various predictors of SCI following extensive TEVAR, as several mechanisms may be involved in the neural tissue responses to anoxia, most notably a combination of reduced blood flow to the spinal cord due to coverage of its collateral network, hemodynamic instability, and infarction due to an embolic mechanism. Individual comorbidities of the patients may also play a role. This chapter details the patient’s medical and anatomic conditions, surgical strategies, and hemodynamic considerations associated with an increased risk of SCI.

3.1. Patient-Related Factors

  • Patient condition
  • In 1681 patients who underwent complex endovascular aortic repair between 2005 and 2020 as part of the US Aortic Research Consortium, age (age ≥70 years (odd ratio (OR) 1.64; 95% confidence interval (CI) 1.63–1.64; p = 0.029)) and a history of peripheral vascular disease (OR 1.65; 95% CI 1.64–1.65; p = 0.034) were significantly associated with SCI [3]. Impaired preoperative renal function (glomerular filtration rate < 60 mL/min/1.73 m2) is also described as a risk factor (OR 2.43; 95% CI 1.18–4.99; p = 0.016) among 243 patients [15].
  • Prior history of aortic repair
  • Several single center studies suggest that prior open infrarenal aortic repair is associated with a higher risk of SCI in the case of proximal thoracic (TEVAR) or thoracoabdominal (TAA) endovascular repair. However, a retrospective review of the Vascular Quality Initiative database found a comparable rate of SCI in 9506 patients treated for TEVAR or TAA and with or without prior repair [16]. The role of prior aortic repair is still under controversy.
  • Atherosclerosis
  • Cumulative cardiovascular risk factors and associated diseases (chronic obstructive pulmonary disease (COPD), obesity, chronic renal insufficiency) have been postulated as markers of widespread peripheral atherosclerotic disease, suggesting that patients may have a compromised collateral network of blood supply to the spinal cord preoperatively. In the end, patients may have a shaggy aorta with a high risk of atheroembolization triggered by intravascular manipulations during surgery. In this case, the Shaggy Aorta Scoring System is a useful method for predicting postoperative embolic complications after TEVAR [17].
  • Patient anatomical factors
  • In the same retrospective review of the Vascular Quality Initiative database of 9506 patients who had undergone extensive endovascular repair, multivariate regression revealed that aortic dissection was an independent factor for postoperative SCI (OR 1.65; 95% CI 1.26–2.16; p < 0.001). However, the main parameter associated with SCI is the extent of the aneurysm and consequently the length of aortic coverage [3,18]. In addition, preoperative occlusion of one or both hypogastric or subclavian arteries contributes to reducing alternative inflow routes to the spinal collateral network. Occlusion of a single collateral bed has long been associated with an increased risk of immediate SCI and poor recovery [8]. Preventive revascularization of the left subclavian artery is recommended (level B, class IIa) to reduce the risk of neurological complications such as stroke and SCI [19].

3.2. Procedure-Related Factors

  • Urgent case
  • Urgent repairs are more likely to lead to hemodynamic instability if the collateral arterial network is still underdeveloped. In fact, in the large DeBakey Medical Center cohort, emergency repairs were found to more than double the risk of SCI (RRR, 2.31; p = 0.002) [20]. An urgent repair in the acute phase of an aortic syndrome appears to be the most dangerous, and its postponement after the 15th day should always be considered when feasible.
  • Length of aortic coverage
  • A large extent of aortic coverage is significantly associated with an increased risk of paraplegia, as shown in a recent large analysis by the US Aortic Consortium (n = 1681 patients; OR 4.79; 95% CI 4.77–4.81; p < 0.001) [3] and a multicenter Italian cohort treated for thoracoabdominal aneurysms of Crawford extents I–III (n = 351 patients; OR 20.90; 95% CI 2.69–162.57; p < 0.004) [18]. Feezor et al. concluded that the risk of SCI is increased by 30% for every 2 cm of additional thoracic aortic coverage [21]. Similarly, Bisdas et al. concluded that each percent of aortic coverage above the superior mesenteric artery leads to a 1.03-fold increase in the risk of SCI [22].
  • Hypotension and hemodynamic instability
  • Prolonged hypotension or hemodynamic instability has been shown to contribute to the risk of immediate or delayed SCI [4,20,23,24]. This risk exists at least in the first few weeks after extensive TEVAR. In a large report that focused on the results of 1114 open type II repairs, SCI occurred in 13.6% of cases, although it should be noted that approximately half of the cases of persistent SCI did not occur immediately after the procedure. Delayed SCI was consistently preceded by hemodynamic instability (hypotension, bleeding, tachyarrhythmia, or heart failure), and hypotension was associated with delayed SCI in 43% [20].

3.3. Prognostic Scores Available

The identification of risk factors for SCI could help to develop a preoperative stratification model to better categorize patients in the high-risk group. This point is essential as it could help to acutely establish the indications for the preventive use of CSFD. Only a few teams have succeeded in developing such a score, which would be of great use in daily practice. In a retrospective cohort, Mousa et al. examined the clinical data of 7889 patients treated for thoracoabdominal endovascular aneurysm repair [25]. All potential demographic and procedural variables previously associated with the occurrence of postoperative paraplegia were tracked. Most procedures were performed in elective surgery (69.6%) for aneurysmal disease (63.4%) in high-volume centers (50%). A total of 166 patients (2.1%) developed permanent SCI (transient 1.5%) with significantly worse postoperative outcomes. The authors calculated a prediction probability for SCI from their original regression (raw score) with 13 items (Table 1). The sum of the items allows the final risk score to be determined and the group to be categorized for SCI.
The authors concluded that the final multivariate logistic regression had good discrimination, a good C-statistic (AUC: 0.792, CI: 0.758–0.826), and good calibration (χ2 1/4 4.9, P 1/4 0.768). In addition, prediction of SCI was consistent when patients were stratified into low, moderate, and high risk (raw scores: 0.786 and 0.738) [23].

4. Bundled Protocol for Spinal Cord Protection

For many years, so-called “bundled” protocols have been used in intensive care units to avoid complications related to the long-term care and management of patients with brain injury (infections, malnutrition, delirium, etc.) [27,28,29,30]. The aim is to combine several multimodal factors to improve the overall prognosis. This approach is comparable to spinal cord protection in aortic repair. The bundled SCI prevention protocol described by Scali et al. is a very good example of the favorable impact of this approach in thoracoabdominal branched or fenestrated endovascular repairs (B/FEVARs) [31]. Implementation of the protocol was associated with a significant decrease in SCI (n = 13 (29%) vs. 3 (2%); p < 0.007), especially in high-risk patients (n = 28 (19%) vs. 2(4%); p = 0.004), and improved 1-year survival (99 ± 1% vs. 90 ± 2% before the protocol; p = 0.05). Several reviews have demonstrated the efficacy of such strategies [32,33,34]. In our opinion, these multimodal protection methods can be divided into three different approaches and a summary of key prevention strategies for spinal cord injury is reported in Table 2.

4.1. Surgical Factor: Staging

Understanding the anatomy and physiology of the collateral network supplying the spinal cord has led to the strategy of the staged endovascular approach [39,40]. It is of utmost importance to give the spinal cord sufficient time to adapt its blood supply to the new condition. To this end, it has been proposed to perform aortic coverage in stages to induce expansion of the collateral network or the formation of new vessels, leading to adequate perfusion of the spinal cord [41,42,43]. The collateral network will form as long as there is sufficient flow and pressure and the pre-existing collateral perfusion is not compromised. This is particularly important if a long aortic segment is to be covered (>200 mm). Interruption of segmental perfusion of the spinal cord induces new collateral vessels in pigs within about 5 days [44,45]. The concept of ischemic preconditioning is a physiologic approach that explains the importance of a staged strategy [46]. The goal is to generate short periods of ischemia that lead to the production of various molecular mechanisms that protect the tissue or organs from a subsequent prolonged ischemic event.
Several staging strategies have been described, most notably covering the descending thoracic aorta with a large TEVAR 6 to 8 weeks before thoracoabdominal repair or delayed implantation of one of the stent-graft limbs, leaving a type Ib endoleak. A randomized, controlled trial of preoperative, minimally invasive, staged segmental arterial coil embolization is currently recruiting and may provide critical elements in favor of this strategy [47].

4.2. Anatomical Approach: Preservation of the Spinal Network

It is now well described that the integrity of the spinal cord may also be maintained by an extensive network of collateral vessels, including contributions from the lumbar arteries and the pelvic circulation [48]. In particular, the left subclavian artery (LSA) and the internal iliac arteries also contribute to the blood supply to the spinal cord by supplying branches that drain into the radiculomedullary vessels [8]. The mechanisms of symptomatic SCI after TEVAR have been studied in the European Registry of Endovascular Aortic Repair Complications (EuREC) [49]. Extensive coverage of intercostal arteries by TEVAR with simultaneous occlusion of at least two vascular territories supplying the spinal cord was found to be highly predictive of SCI, especially in combination with persistent intraoperative hypotension.
Risk factors for SCI include coverage of the left subclavian artery (LSA) and impairment (or sacrifice) of distal collateral inflow, including the intercostal and lumbar segmental arteries, hypogastric arteries, and sacral arteries. In this context, a history of PAD and other cardiovascular risk factors (diabetes mellitus, hypertension, renal disease, etc.) represents an important associated factor which probably explains the consequences of SCI. Therefore, every effort must be made to achieve early reperfusion of the pelvic and lower limbs and preservation or revascularization of the LSA and internal iliac artery. The contribution of the collateral network arising from the LSA and internal iliac arteries explains why patients have poorer outcomes when one or more of these branches are occluded [50].

4.3. Medical Approach: Optimization of Spinal Cord Oxygenation

The short duration of low spinal cord blood flow associated with SCI suggests that medical therapy with hemodynamic and metabolic interventions lasting only 24–72 h may allow routine preservation of normal spinal cord function despite the sacrifice of all vascular networks via endovascular repair of large TAAs.
  • Permissive hypertension and spinal cord perfusion pressure (SCPP)
  • Since the irreversible damage to the spinal cord occurs 12 to 48 h after surgery, an immediate response is imperative to try to reverse spinal cord suffering and permanent impairment. Thus, increasing mean arterial pressure (MAP) appears to be the first immediate action that should be taken without further delay given the close relationship between systemic blood pressure and spinal cord perfusion [51]. In general, vasopressor agents such as noradrenaline are administered to maintain a target MAP of 80–100 mmHg and to ensure an SCPP of at least 70 mmHg [52].
SCPP = MAPd − (CSFP or CVP [whichever is greater])
  • SCPP: spinal cord perfusion pressure; MAPd: distal mean aortic pressure; CSFP: cerebrospinal fluid pressure; CVP: central venous pressure.
  • Failure to maintain a patient’s preoperative baseline arterial pressure in the early postoperative period is strongly associated with delayed postoperative SCI [53]. MAP can be further increased in 5–10 mmHg steps in case of persisting SCI.
  • Active CSFD can also rapidly improve PPM by lowering SCPP and must be considered in urgent cases.
  • Secondary spinal cord injuries (SSCIs)
  • Irreversible, systemic secondary SCI is a major prognostic factor in the prevention of neurological sequelae following a lesion process. It refers to the changes that develop over a period of time (from hours to days) after the primary spinal injury. This includes a whole cascade of cellular, chemical, tissue, or vascular changes in the spine that contribute to further destruction of the spinal tissue [54]. This concept was originally developed for traumatic brain injury, but can be extended to any central neurological damage, including SCI in aortic endovascular surgery. These lesions, termed “secondary,” may be intraspinal in origin, a consequence of metabolic and inflammatory disturbances associated with the primary ischemia, or they may be systemic in origin, when failure of vital cardiorespiratory functions leads to spinal ischemia [55]. This is referred to as secondary spinal injury of systemic origin (Table 3). This concept explains the higher proportion of SCI in patients with COPD (hypoxemia) or transfusion of packed red blood cells (anemia):
    -
    Oxygen
    • Any hypoxemia should be considered potentially dangerous. Maintaining a PaO2 of at least 60 mmHg (SpO2 > 95%) is therefore a primary goal.
    -
    Hemoglobin
    • Evidence-based recommendations for patient blood management have recently been published [56]. A formal program must be implemented for every anemic patient prior to complex endovascular aortic repair. A hemoglobin concentration of 7–8 g/dL is the transfusion threshold that applies in intensive care units for cardiac surgery or critically ill patients. However, for patients with acute central nervous system injury, there is a lack of high-quality published data. In the absence of a clear recommendation, it is usual to consider a transfusion threshold of 10 g/dL in case of SCI [24].

4.4. Neuromonitoring

All efforts are now also focused on the early detection of spinal cord disorders. Time is of the essence when the spinal cord is suffering, and early diagnosis may change the patient’s functional prognosis, as irreversible damage occurs as early as 12 to 48 h postoperatively [57]. To this end, perioperative neurophysiologic monitoring methods are being developed.
  • Intraoperative neuromonitoring
  • This technology, when available, is part of the strategy to reduce SCI real-time identification of motor or sensory neurological dysfunction so that immediate action can be taken to improve cord perfusion. In case of peroperative alteration of the motor (anterior cord) or sensory (dorsal part of the evoked potential of the spinal cord (MEP)) function, the first strategy is to increase the mean arterial pressure to reverse the alteration and return to reference values. If hemodynamic optimization is not sufficient, revascularization of the pelvis and lower limbs may be proposed if technically feasible, and finally early interruption of the procedure if possible.
  • Biomarkers
  • For early detection of SCI, real-time biomarkers may be of utmost importance, particularly in the perioperative setting when the patient is under general anesthesia and cannot be examined clinically. Cerebrospinal fluid (CSF) appears to be the fluid of choice for this purpose, as it continuously interacts with the spinal cord tissue and is therefore predestined to reflect metabolic changes. Research about proteomic profiling from CSF has shown that these markers are released too long after the onset of acute SCI and therefore cannot be used. Studies on serum markers have also found a slow and delayed release into the bloodstream [58].
  • In a more recent work, changes in sensitive anaerobic metabolites with early release were studied for the first time. The authors used microdialysis of CSF during intraoperative procedures to detect severe disturbances in neurological energy metabolism in real time: lactate, lactate/pyruvate ratio, and glucose and glycerol levels. The authors reported a correlation between an increase in the lactate/pyruvate ratio, indicating the onset of anaerobic metabolism, and >50% change in motor evoked potential (MEP) in two patients. This could be a promising tool for the early detection of SCI in the future [57].

4.5. Pharmacologic Adjuncts

These include many pharmacological agents with antiedematous effects, but there are no prospective studies and they are mainly described in cases of open repair. The principle is to reduce the spinal cord edema caused by ischemia (steroids, mannitol), and to reduce the amounts of excitatory amino acids that play a role in spinal cord injury (naloxone) [33,45,59].

4.6. Basic Research on Early Detection of SCI

  • Neuromonitoring
  • Due to the risk of false-positive results in neuromonitoring, experimental research is being conducted to improve the technique. Transesophageal MEP has been reported to provide a shorter response time in animal models [60]. Research into the possibility of stimulating and recording intercostal nerve activity has also been published [61].
  • Biomarkers
  • The focus of current experiments on biomarkers is on structural proteins that are released into the cerebrospinal fluid and bloodstream as a result of damage to nerve tissue. However, despite the extensive literature on this topic, the diagnostic possibilities are currently limited. It has been proposed that in the future a multimodal approach be adopted to optimize spinal cord protection, combining near-infrared spectroscopy of the collateral network, neuromonitoring, and a combination of biomarkers [11].

5. Cerebrospinal Fluid Drainage (CSFD)

The CSFD technique was first used in experimental laboratories in the 1960s. Currently, the use of CSFD is controversial because the rate of serious complications associated with drain placement is alarmingly high and the evidence for its use in endovascular strategies is weak. Catheter-related complications are now well recognized and have probably been underestimated compared with the benefits that have been demonstrated in extensive open aortic surgery with proximal clamping. In the era of “endovascular-only” treatment, the indication probably needs to be more targeted and management ensured by experienced teams. In fact, several high-volume centers in different countries now recommend the curative use of CSFD, which is only used as a rescue measure when symptoms occur. However, early diagnosis of SCI and urgent CSF aspiration are of paramount importance and not always feasible in the absence of preoperative drainage, especially in cases of delayed symptomatology. Consequently, the preventive use of CSF extraction is nowadays a second-choice strategy and should be reserved for the most vulnerable cases.

5.1. Rational

Little is known about the inflammatory cascade and peri-cord edema that occur after extensive aortic coverage and spinal ischemia. The basic idea of CSF drainage is to reduce CSF pressure and thereby optimize perfusion pressure in the spinal cord by improving blood flow to the spinal cord. It is known that increasing MAP and lowering spinal CSF pressure are the most important maneuvers to reverse SCI. The most common level for placement is L4–L5.

5.2. Risk of CSFD and Contraindications

Several high-volume aortic centers have reported a significant dysfunction rate of 16% from a preemptive CSFD and frequent minor complications [62]. Most importantly, serious drainage complications have been consistently reported in the literature, with a rate of 3%.
The most important complication of CSF drainage is spinal hematoma, which can lead to catastrophic paraplegia. For this reason, special attention should be paid to the patient’s medication and coagulation prior to any extensive repair where there is a risk for SCI. A Delphi consensus recommends switching to aspirin for all patients on P2Y12 inhibitors or dual antiplatelet therapy. For patients on oral anticoagulation, discontinuation 2 to 5 days prior to surgery is mandatory [63], and also depends on the type of anticoagulant used and patient characteristics such as renal function.
The suggestion that up to 20% of paraplegias are due to spinal hematomas has reversed the trend in several large-volume centers to use drainage as a prophylactic strategy [64]. Particular caution should be exercised when considering prophylactic CSF drainage in patients at high risk of technical difficulties with drain insertion or in patients who have a low platelet count or high INR preoperatively. Screening for blood coagulation disorders should be carried out. In our experience, patients with degenerative diseases of the lumbar spine or under long-term curative anticoagulation are contraindicated for prophylactic CSF removal. Perioperative medication should be adapted to the recommendations in order to avoid further complications if curative CSFD is required.

5.3. Nantes University Protocol for CSFD Use

This alarming rate of paraplegia associated with CSFD-induced spinal cord injury has led to a shift from a preventive approach to a bail-out technique in several high-volume centers around the world. However, when changing strategies to use CSF drainage only as a rescue measure, several questions need to be evaluated: how well and quickly the patient can be neurologically assessed postoperatively, how quickly a rescue drainage can be performed by an expert, and how experienced the team is with drain placement. After all, if there is no monitoring of intraspinal pressure, any neurological signs must be recognized and treated immediately.
For this reason, we introduced a decision algorithm at our center several years ago to better define the risk of SCI and selective CSFD strategies. Taking into account the main preoperative surgical factors reported in the literature (Table 4), we can define three risk levels for the development of SCI and plan our prevention strategy based on the total number of risk factors (Figure 4) and the contraindication for CSFD. In our experience, patients with long-term anticoagulation, patients with unfavorable spinal anatomy, and patients with mental disorders have a high risk of CSFD complications and are contraindicated for preventive CSFD.
This approach may differ slightly from current recommendations. For example, the European Society of Vascular Surgery recommends placement of a CSFD with >200 mm coverage of the thoracic aorta or a previous AAA repair (class IIb, level of evidence C) [37]. In our protocol, we consider this situation as an intermediate neurological risk and refrain from prophylactic CSFD in the preoperative phase.
It is common practice to reduce or discontinue antihypertensive medications (with the exception of beta-blockers) for 48 h prior to endovascular aortic repair. We also recommend suspending antihypertensive medications for up to 30 days after the procedure.

5.4. Our Initial Experience after the Implementation of This Protective Protocol

We recently published our first experiences following the introduction of the protection protocol described above. From 2016 to 2021, we retrospectively analyzed our outcomes in terms of spinal cord injury (SCI rate and CFSD-related complications) in patients who underwent consecutive endovascular treatment for TAA disease. Patients were categorized as high risk (≥2 factors), intermediate risk (1 factor), or low risk (0 factors). Only high-risk patients without contraindications underwent prophylactic CSFD placement.
Among 181 patients (124 men; 69.6 years), 130 (69%) were treated for aneurysms (n = 24 thoracic, n = 28 Crawford 1-2-3, and n = 78 Crawford 4/pararenal); 35 (19.9%) for chronic aneurysmal dissections; and 16 (8.8%) for acute complicated type B dissections. Interventions were staged in 31 (17.2%) cases and consisted of 74 (41%) TEVARs and 107 (59%) F-BEVARs. Sixty-nine (38.1%) patients were identified as being at high risk of SCI, and sixty-four of them underwent prophylactic CFSD (four failures and one contraindication). SCI occurred in eight cases (four paraparesis cases and four paraplegias, two of which were permanent), of which three received prophylactic CSFD and five received rescue drainage. In addition, four patients developed SCI (intradural hematoma) in connection with the prophylactic CSFD, which led to one paraparesis and three paraplegias. Other CSFD-related complications were mild (6) or moderate (2), totaling 12 complications (17%). Factors associated with severe drainage-related complications were curative anticoagulation 36 h after drain removal (n = 1), multiple punctures (n = 1), platelet count < 100,000 at drain removal (n = 1), and bipolar disorder (n = 2). A total of four patients had permanent paraplegia and one had sphincter dysfunction at the last follow-up. The average follow-up time was 17 months. Mortality was 4.4% at 30 days and 13.3% at 18 months, including three (1.6%) aortic-related deaths [65].

6. Conclusions

Clinical research in the field of spinal cord injury prevention is struggling to keep pace with advances in surgical techniques, particularly with the advent of endovascular repair. Recent data clearly demonstrate the adverse effects and morbidity caused by drainage catheters, particularly in low-volume aortic centers. There is now an urgent need to rigorously validate the interest of lumbar drainage using pragmatic algorithms and suggest a different strategy depending on the team’s experience and the patient’s risk factors. With this considered and sensible approach, it is likely that the indications for preventive CSFD will be greatly reduced in the near future. However, this should be confirmed in future studies or large registries. Above all, the complexity not only of the procedure but also of periprocedural decision making should ensure that these procedures are only performed in high-volume centers.

Author Contributions

L.B., O.B., S.E.B. and B.M. have approved the submitted version and agree to be personally accountable for the authors’ own contributions and for ensuring that questions related to the accuracy or integrity of any part of the work are answered. S.E.B. is the medical illustrator of the figures. All authors have read and agreed to the published version of the manuscript.

Funding

This research received no external funding.

Data Availability Statement

Not applicable.

Conflicts of Interest

L.B.: grant from Baxter™. B.M.: consulting fees from Cook Medical, Philips; speaking fees from Cook Medical, Gore, Cydar; proctoring fees from Cook Medical. The remaining author declare no conflicts of interest.

References

  1. World Health Organization. International Perspectives on Spinal Cord Injury. Available online: https://www.who.int/publications-detail-redirect/international-perspectives-on-spinal-cord-injury (accessed on 5 February 2023).
  2. Adams, H.D.; van Geertruyden, H.H. Neurologic Complications of Aortic Surgery. Ann. Surg. 1956, 144, 574. [Google Scholar] [CrossRef] [PubMed]
  3. Aucoin, V.J.; Motyl, C.M.; Novak, Z.; Eagleton, M.J.; Farber, M.A.; Gasper, W.; Oderich, G.S.; Mendes, B.; Schanzer, A.; Tenorio, E.; et al. Predictors and Outcomes of Spinal Cord Injury Following Complex Branched/Fenestrated Endovascular Aortic Repair in the US Aortic Research Consortium. J. Vasc. Surg. 2023, 77, 1578–1587. [Google Scholar] [CrossRef] [PubMed]
  4. Scali, S.T.; Giles, K.A.; Wang, G.J.; Kubilis, P.; Neal, D.; Huber, T.S.; Upchurch, G.R.; Siracuse, J.J.; Shutze, W.P.; Beck, A.W. National Incidence, Mortality Outcomes, and Predictors of Spinal Cord Ischemia after Thoracic Endovascular Aortic Repair. J. Vasc. Surg. 2020, 72, 92–104. [Google Scholar] [CrossRef] [PubMed]
  5. Kitpanit, N.; Ellozy, S.H.; Connolly, P.H.; Agrusa, C.J.; Lichtman, A.D.; Schneider, D.B. Risk Factors for Spinal Cord Injury and Complications of Cerebrospinal Fluid Drainage in Patients Undergoing Fenestrated and Branched Endovascular Aneurysm Repair. J. Vasc. Surg. 2021, 73, 399–409.e1. [Google Scholar] [CrossRef] [PubMed]
  6. Aucoin, V.J.; Eagleton, M.J.; Farber, M.A.; Oderich, G.S.; Schanzer, A.; Timaran, C.H.; Schneider, D.B.; Sweet, M.P.; Beck, A.W. Spinal Cord Protection Practices Used during Endovascular Repair of Complex Aortic Aneurysms by the U.S. Aortic Research Consortium. J. Vasc. Surg. 2021, 73, 323–330. [Google Scholar] [CrossRef] [PubMed]
  7. Dias-Neto, M.; Tenorio, E.R.; Huang, Y.; Jakimowicz, T.; Mendes, B.C.; Kölbel, T.; Sobocinski, J.; Bertoglio, L.; Mees, B.; Gargiulo, M.; et al. Comparison of Single- and Multistage Strategies during Fenestrated-Branched Endovascular Aortic Repair of Thoracoabdominal Aortic Aneurysms. J. Vasc. Surg. 2023, 77, 1588–1597.e4. [Google Scholar] [CrossRef] [PubMed]
  8. Eagleton, M.J.; Shah, S.; Petkosevek, D.; Mastracci, T.M.; Greenberg, R.K. Hypogastric and Subclavian Artery Patency Affects Onset and Recovery of Spinal Cord Ischemia Associated with Aortic Endografting. J. Vasc. Surg. 2014, 59, 89–95. [Google Scholar] [CrossRef]
  9. Arora, L.; Hosn, M.A. Spinal Cord Perfusion Protection for Thoraco-Abdominal Aortic Aneurysm Surgery. Curr. Opin. Anesthesiol. 2019, 32, 72. [Google Scholar] [CrossRef]
  10. Awad, H.; Ramadan, M.E.; El Sayed, H.F.; Tolpin, D.A.; Tili, E.; Collard, C.D. Spinal Cord Injury after Thoracic Endovascular Aortic Aneurysm Repair. Can. J. Anesth. 2017, 64, 1218–1235. [Google Scholar] [CrossRef]
  11. Khachatryan, Z.; Haunschild, J.; von Aspern, K.; Borger, M.A.; Etz, C.D. Ischemic Spinal Cord Injury—Experimental Evidence and Evolution of Protective Measures. Ann. Thorac. Surg. 2022, 113, 1692–1702. [Google Scholar] [CrossRef]
  12. Melissano, G.; Bertoglio, L.; Civelli, V.; Moraes Amato, A.C.; Coppi, G.; Civilini, E.; Calori, G.; De Cobelli, F.; Del Maschio, A.; Chiesa, R. Demonstration of the Adamkiewicz Artery by Multidetector Computed Tomography Angiography Analysed with the Open-Source Software OsiriX. Eur. J. Vasc. Endovasc. Surg. 2009, 37, 395–400. [Google Scholar] [CrossRef] [PubMed]
  13. Tanaka, H.; Minatoya, K.; Matsuda, H.; Sasaki, H.; Iba, Y.; Oda, T.; Kobayashi, J. Embolism Is Emerging as a Major Cause of Spinal Cord Injury after Descending and Thoracoabdominal Aortic Repair with a Contemporary Approach: Magnetic Resonance Findings of Spinal Cord Injury. Interact. Cardiovasc. Thorac. Surg. 2014, 19, 205–210. [Google Scholar] [CrossRef] [PubMed]
  14. Vargas, M.I.; Gariani, J.; Sztajzel, R.; Barnaure-Nachbar, I.; Delattre, B.M.; Lovblad, K.O.; Dietemann, J.-L. Spinal Cord Ischemia: Practical Imaging Tips, Pearls, and Pitfalls. Am. J. Neuroradiol. 2015, 36, 825–830. [Google Scholar] [CrossRef] [PubMed]
  15. Spanos, K.; Kölbel, T.; Kubitz, J.C.; Wipper, S.; Konstantinou, N.; Heidemann, F.; Rohlffs, F.; Debus, S.E.; Tsilimparis, N. Risk of Spinal Cord Ischemia after Fenestrated or Branched Endovascular Repair of Complex Aortic Aneurysms. J. Vasc. Surg. 2019, 69, 357–366. [Google Scholar] [CrossRef] [PubMed]
  16. Chen, S.; Rokosh, R.S.; Smith, D.E.; Maldonado, T.S.; Cayne, N.S.; Jacobowitz, G.R.; Rockman, C.B.; Patel, V.I.; Veith, F.J.; Galloway, A.C.; et al. Prior Infrarenal Aortic Surgery Is Not Associated with Increased Risk of Spinal Cord Ischemia after Thoracic Endovascular Aortic Repair and Complex Endovascular Aortic Repair. J. Vasc. Surg. 2022, 75, 1152–1162.e6. [Google Scholar] [CrossRef]
  17. Maeda, K.; Ohki, T.; Kanaoka, Y.; Shukuzawa, K.; Baba, T.; Momose, M. A Novel Shaggy Aorta Scoring System to Predict Embolic Complications Following Thoracic Endovascular Aneurysm Repair. Eur. J. Vasc. Endovasc. Surg. 2020, 60, 57–66. [Google Scholar] [CrossRef] [PubMed]
  18. Rinaldi, E.; Melloni, A.; Gallitto, E.; Fargion, A.; Isernia, G.; Kahlberg, A.; Bertoglio, L.; Faggioli, G.; Lenti, M.; Pratesi, C.; et al. Spinal Cord Ischemia After Thoracoabdominal Aortic Aneurysms Endovascular Repair: From the Italian Multicenter Fenestrated/Branched Endovascular Aneurysm Repair Registry. J. Endovasc. Ther. 2023, 30, 281–288. [Google Scholar] [CrossRef]
  19. Piazza, M.; Zavatta, M.; Lamaina, M.; Taglialavoro, J.; Squizzato, F.; Grego, F.; Antonello, M. Early Outcomes of Routine Delayed Shunting in Carotid Endarterectomy for Asymptomatic Patients. Eur. J. Vasc. Endovasc. Surg. 2018, 56, 334–341. [Google Scholar] [CrossRef]
  20. Coselli, J.S.; Green, S.Y.; Price, M.D.; Zhang, Q.; Preventza, O.; de la Cruz, K.I.; Whitlock, R.; Amarasekara, H.S.; Woodside, S.J.; Perez-Orozco, A.; et al. Spinal Cord Deficit after 1114 Extent II Open Thoracoabdominal Aortic Aneurysm Repairs. J. Thorac. Cardiovasc. Surg. 2020, 159, 1–13. [Google Scholar] [CrossRef]
  21. Feezor, R.J.; Martin, T.D.; Hess, P.J.; Daniels, M.J.; Beaver, T.M.; Klodell, C.T.; Lee, W.A. Extent of Aortic Coverage and Incidence of Spinal Cord Ischemia After Thoracic Endovascular Aneurysm Repair. Ann. Thorac. Surg. 2008, 86, 1809–1814. [Google Scholar] [CrossRef]
  22. Bisdas, T.; Panuccio, G.; Sugimoto, M.; Torsello, G.; Austermann, M. Risk Factors for Spinal Cord Ischemia after Endovascular Repair of Thoracoabdominal Aortic Aneurysms. J. Vasc. Surg. 2015, 61, 1408–1416. [Google Scholar] [CrossRef]
  23. Chang, C.K.; Chuter, T.A.M.; Reilly, L.M.; Ota, M.K.; Furtado, A.; Bucci, M.; Wintermark, M.; Hiramoto, J.S. Spinal Arterial Anatomy and Risk Factors for Lower Extremity Weakness Following Endovascular Thoracoabdominal Aortic Aneurysm Repair with Branched Stent-Grafts. J. Endovasc. Ther. 2008, 15, 356–362. [Google Scholar] [CrossRef] [PubMed]
  24. Etz, C.D.; Weigang, E.; Hartert, M.; Lonn, L.; Mestres, C.A.; Di Bartolomeo, R.; Bachet, J.E.; Carrel, T.P.; Grabenwöger, M.; Schepens, M.A.A.M.; 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, 943–957. [Google Scholar] [CrossRef] [PubMed]
  25. Mousa, A.Y.; Morcos, R.; Broce, M.; Bates, M.C.; AbuRahma, A.F. New Preoperative Spinal Cord Ischemia Risk Stratification Model for Patients Undergoing Thoracic Endovascular Aortic Repair. Vasc. Endovascular Surg. 2020, 54, 487–496. [Google Scholar] [CrossRef] [PubMed]
  26. Khemlani, K.H.; Schurink, G.W.; Buhre, W.; Schreiber, J.U. Cerebrospinal Fluid Drainage in Thoracic and Thoracoabdominal Endovascular Aortic Repair: A Survey of Current Clinical Practice in European Medical Centers. J. Cardiothorac. Vasc. Anesth. 2022, 36, 1318–1325. [Google Scholar] [CrossRef] [PubMed]
  27. Nakano, H.; Naraba, H.; Hashimoto, H.; Mochizuki, M.; Takahashi, Y.; Sonoo, T.; Ogawa, Y.; Matsuishi, Y.; Shimojo, N.; Inoue, Y.; et al. Novel Protocol Combining Physical and Nutrition Therapies, Intensive Goal-Directed REhabilitation with Electrical Muscle Stimulation and Nutrition (IGREEN) Care Bundle. Crit. Care 2021, 25, 415. [Google Scholar] [CrossRef] [PubMed]
  28. Klompas, M.; Li, L.; Kleinman, K.; Szumita, P.M.; Massaro, A.F. Associations Between Ventilator Bundle Components and Outcomes. JAMA Intern. Med. 2016, 176, 1277. [Google Scholar] [CrossRef] [PubMed]
  29. Barr, J.; Pandharipande, P.P. The Pain, Agitation, and Delirium Care Bundle: Synergistic Benefits of Implementing the 2013 Pain, Agitation, and Delirium Guidelines in an Integrated and Interdisciplinary Fashion. Crit. Care Med. 2013, 41, S99–S115. [Google Scholar] [CrossRef]
  30. Roquilly, A.; Cinotti, R.; Jaber, S.; Vourc’h, M.; Pengam, F.; Mahe, P.J.; Lakhal, K.; Demeure Dit Latte, D.; Rondeau, N.; Loutrel, O.; et al. Implementation of an Evidence-Based Extubation Readiness Bundle in 499 Brain-Injured Patients. a before-after Evaluation of a Quality Improvement Project. Am. J. Respir. Crit. Care Med. 2013, 188, 958–966. [Google Scholar] [CrossRef]
  31. Scali, S.T.; Kim, M.; Kubilis, P.; Feezor, R.J.; Giles, K.A.; Miller, B.; Fatima, J.; Huber, T.S.; Berceli, S.A.; Back, M.; et al. Implementation of a Bundled Protocol Significantly Reduces Risk of Spinal Cord Ischemia after Branched or Fenestrated Endovascular Aortic Repair. J. Vasc. Surg. 2018, 67, 409–423.e4. [Google Scholar] [CrossRef]
  32. Dijkstra, M.L.; Vainas, T.; Zeebregts, C.J.; Hooft, L.; van der Laan, M.J. Editor’s Choice—Spinal Cord Ischaemia in Endovascular Thoracic and Thoraco-Abdominal Aortic Repair: Review of Preventive Strategies. Eur. J. Vasc. Endovasc. Surg. 2018, 55, 829–841. [Google Scholar] [CrossRef] [PubMed]
  33. Miller, L.K.; Patel, V.I.; Wagener, G. Spinal Cord Protection for Thoracoabdominal Aortic Surgery. J. Cardiothorac. Vasc. Anesth. 2022, 36, 577–586. [Google Scholar] [CrossRef] [PubMed]
  34. Parotto, M.; Ouzounian, M.; Djaiani, G. Spinal Cord Protection in Elective Thoracoabdominal Aortic Procedures. J. Cardiothorac. Vasc. Anesth. 2019, 33, 200–208. [Google Scholar] [CrossRef] [PubMed]
  35. Isselbacher, E.M.; Preventza, O.; Hamilton Black, J.; Augoustides, J.G.; Beck, A.W.; Bolen, M.A.; Braverman, A.C.; Bray, B.E.; Brown-Zimmerman, M.M.; Chen, E.P.; et al. 2022 ACC/AHA Guideline for the Diagnosis and Management of Aortic Disease: A Report of the American Heart Association/American College of Cardiology Joint Committee on Clinical Practice Guidelines. Circulation 2022, 146, e334–e482. [Google Scholar] [CrossRef] [PubMed]
  36. Czerny, M.; Schmidli, J.; Adler, S.; van den Berg, J.C.; Bertoglio, L.; Carrel, T.; Chiesa, R.; Clough, R.E.; Eberle, B.; Etz, C.; et al. Editor’s Choice—Current Options and Recommendations for the Treatment of Thoracic Aortic Pathologies Involving the Aortic Arch: An Expert Consensus Document of the European Association for Cardio-Thoracic Surgery (EACTS) & the European Society for Vascular Surgery (ESVS). Eur. J. Vasc. Endovasc. Surg. 2019, 57, 165–198. [Google Scholar] [CrossRef]
  37. Riambau, V.; Böckler, D.; Brunkwall, J.; Cao, P.; Chiesa, R.; Coppi, G.; Czerny, M.; Fraedrich, G.; Haulon, S.; Jacobs, M.J.; et al. Editor’s Choice—Management of Descending Thoracic Aorta Diseases: Clinical Practice Guidelines of the European Society for Vascular Surgery (ESVS). Eur. J. Vasc. Endovasc. Surg. 2017, 53, 4–52. [Google Scholar] [CrossRef]
  38. Erbel, R.; Aboyans, V.; Boileau, C.; Bossone, E.; Bartolomeo, R.D.; Eggebrecht, H.; Evangelista, A.; Falk, V.; Frank, H.; Gaemperli, O.; et al. 2014 ESC Guidelines on the Diagnosis and Treatment of Aortic Diseases—Document Covering Acute and Chronic Aortic Diseases of the Thoracic and Abdominal Aorta of the adult the Task Force for the Diagnosis and Treatment of Aortic Diseases of the European Society of Cardiology (ESC). Eur. Heart J. 2014, 35, 2873–2926. [Google Scholar] [CrossRef]
  39. Etz, C.D.; Kari, F.A.; Mueller, C.S.; Silovitz, D.; Brenner, R.M.; Lin, H.-M.; Griepp, R.B. The Collateral Network Concept: A Reassessment of the Anatomy of Spinal Cord Perfusion. J. Thorac. Cardiovasc. Surg. 2011, 141, 1020–1028. [Google Scholar] [CrossRef]
  40. Etz, C.D.; Kari, F.A.; Mueller, C.S.; Brenner, R.M.; Lin, H.-M.; Griepp, R.B. The Collateral Network Concept: Remodeling of the Arterial Collateral Network after Experimental Segmental Artery Sacrifice. J. Thorac. Cardiovasc. Surg. 2011, 141, 1029–1036. [Google Scholar] [CrossRef]
  41. Bischoff, M.S.; Scheumann, J.; Brenner, R.M.; Ladage, D.; Bodian, C.A.; Kleinman, G.; Ellozy, S.H.; Luozzo, G.D.; Etz, C.D.; Griepp, R.B. Staged Approach Prevents Spinal Cord Injury in Hybrid Surgical-Endovascular Thoracoabdominal Aortic Aneurysm Repair: An Experimental Model. Ann. Thorac. Surg. 2011, 92, 138–146. [Google Scholar] [CrossRef]
  42. Zoli, S.; Etz, C.D.; Roder, F.; Brenner, R.M.; Bodian, C.A.; Kleinman, G.; Luozzo, G.D.; Griepp, R.B. Experimental Two-Stage Simulated Repair of Extensive Thoracoabdominal Aneurysms Reduces Paraplegia Risk. Ann. Thorac. Surg. 2010, 90, 722–729. [Google Scholar] [CrossRef] [PubMed]
  43. Etz, C.D.; Zoli, S.; Mueller, C.S.; Bodian, C.A.; Luozzo, G.D.; Lazala, R.; Plestis, K.A.; Griepp, R.B. Staged Repair Significantly Reduces Paraplegia Rate after Extensive Thoracoabdominal Aortic Aneurysm Repair. J. Thorac. Cardiovasc. Surg. 2010, 139, 1464–1472. [Google Scholar] [CrossRef] [PubMed]
  44. Etz, C.D.; Homann, T.M.; Plestis, K.A.; Zhang, N.; Luehr, M.; Weisz, D.J.; Kleinman, G.; Griepp, R.B. Spinal Cord Perfusion after Extensive Segmental Artery Sacrifice: Can Paraplegia Be Prevented? Eur. J. Cardiothorac. Surg. 2007, 31, 643–648. [Google Scholar] [CrossRef] [PubMed]
  45. Tenorio, E.R.; Eagleton, M.J.; Kärkkäinen, J.M.; Oderich, G.S. Prevention of Spinal Cord Injury during Endovascular Thoracoabdominal Repair. J. Cardiovasc. Surg. 2019, 60, 1629. [Google Scholar] [CrossRef] [PubMed]
  46. Etz, C.D.; Debus, E.S.; Mohr, F.-W.; Kölbel, T. First-in-Man Endovascular Preconditioning of the Paraspinal Collateral Network by Segmental Artery Coil Embolization to Prevent Ischemic Spinal Cord Injury. J. Thorac. Cardiovasc. Surg. 2015, 149, 1074–1079. [Google Scholar] [CrossRef] [PubMed]
  47. Petroff, D.; Czerny, M.; Kölbel, T.; Melissano, G.; Lonn, L.; Haunschild, J.; Aspern, K.; Neuhaus, P.; Pelz, J.; Epstein, D.M.; et al. Paraplegia Prevention in Aortic Aneurysm Repair by Thoracoabdominal Staging with ‘Minimally Invasive Staged Segmental Artery Coil Embolisation’ (MIS2ACE): Trial Protocol for a Randomised Controlled Multicentre Trial. BMJ Open 2019, 9, e025488. [Google Scholar] [CrossRef] [PubMed]
  48. Jacobs, M.J.; Elenbaas, T.W.; Schurink, G.W.H.; Mess, W.H.; Mochtar, B. Assessment of Spinal Cord Integrity during Thoracoabdominal Aortic Aneurysm Repair. Ann. Thorac. Surg. 2002, 74, S1864–S1866. [Google Scholar] [CrossRef]
  49. Czerny, M.; Eggebrecht, H.; Sodeck, G.; Verzini, F.; Cao, P.; Maritati, G.; Riambau, V.; Beyersdorf, F.; Rylski, B.; Funovics, M.; et al. Mechanisms of Symptomatic Spinal Cord Ischemia After TEVAR: Insights from the European Registry of Endovascular Aortic Repair Complications (EuREC). J. Endovasc. Ther. 2012, 19, 37–43. [Google Scholar] [CrossRef]
  50. Rizvi, A.Z.; Murad, M.H.; Fairman, R.M.; Erwin, P.J.; Montori, V.M. The Effect of Left Subclavian Artery Coverage on Morbidity and Mortality in Patients Undergoing Endovascular Thoracic Aortic Interventions: A Systematic Review and Meta-Analysis. J. Vasc. Surg. 2009, 50, 1159–1169. [Google Scholar] [CrossRef]
  51. Kise, Y.; Kuniyoshi, Y.; Inafuku, H.; Nagano, T.; Hirayasu, T.; Yamashiro, S. Directly Measuring Spinal Cord Blood Flow and Spinal Cord Perfusion Pressure via the Collateral Network: Correlations with Changes in Systemic Blood Pressure. J. Thorac. Cardiovasc. Surg. 2015, 149, 360–366. [Google Scholar] [CrossRef]
  52. Estrera, A.L.; Miller, C.C.; Huynh, T.T.T.; Porat, E.; Safi, H.J. Neurologic Outcome after Thoracic and Thoracoabdominal Aortic Aneurysm Repair. Ann. Thorac. Surg. 2001, 72, 1225–1231. [Google Scholar] [CrossRef] [PubMed]
  53. Etz, C.D.; Luehr, M.; Kari, F.A.; Bodian, C.A.; Smego, D.; Plestis, K.A.; Griepp, R.B. Paraplegia after Extensive Thoracic and Thoracoabdominal Aortic Aneurysm Repair: Does Critical Spinal Cord Ischemia Occur Postoperatively? J. Thorac. Cardiovasc. Surg. 2008, 135, 324–330. [Google Scholar] [CrossRef] [PubMed]
  54. Anwar, M.A.; Al Shehabi, T.S.; Eid, A.H. Inflammogenesis of Secondary Spinal Cord Injury. Front. Cell. Neurosci. 2016, 10, 98. [Google Scholar] [CrossRef]
  55. Jones, P.A.; Andrews, P.J.; Midgley, S.; Anderson, S.I.; Piper, I.R.; Tocher, J.L.; Housley, A.M.; Corrie, J.A.; Slattery, J.; Dearden, N.M. Measuring the Burden of Secondary Insults in Head-Injured Patients during Intensive Care. J. Neurosurg. Anesthesiol. 1994, 6, 4–14. [Google Scholar] [CrossRef]
  56. Mueller, M.M.; Remoortel, H.V.; Meybohm, P.; Aranko, K.; Aubron, C.; Burger, R.; Carson, J.L.; Cichutek, K.; Buck, E.D.; Devine, D.; et al. Patient Blood Management: Recommendations From the 2018 Frankfurt Consensus Conference. JAMA J. Am. Med. Assoc. 2019, 321, 983–997. [Google Scholar] [CrossRef] [PubMed]
  57. Simoniuk, U.D.; Haunschild, J.; von Aspern, K.; Boschmann, M.; Klug, L.; Khachatryan, Z.; Bianchi, E.; Ossmann, S.; Oo, A.Y.; Borger, M.A.; et al. Near Real-Time Bedside Detection of Spinal Cord Ischaemia during Aortic Repair by Microdialysis of the Cerebrospinal Fluid. Eur. J. Cardiothorac. Surg. 2020, 58, 629–637. [Google Scholar] [CrossRef]
  58. Püschel, A.; Ebel, R.; Fuchs, P.; Hofmann, J.; Schubert, J.K.; Roesner, J.P.; Bergt, S.; Wree, A.; Vollmar, B.; Klar, E.; et al. Can Recognition of Spinal Ischemia Be Improved? Application of Motor-Evoked Potentials, Serum Markers, and Breath Gas Analysis in an Acutely Instrumented Pig Model. Ann. Vasc. Surg. 2018, 49, 191–205. [Google Scholar] [CrossRef]
  59. Hiratzka, L.F.; Bakris, G.L.; Beckman, J.A.; Bersin, R.M.; Carr, V.F.; Casey, D.E.; Eagle, K.A.; Hermann, L.K.; Isselbacher, E.M.; Kazerooni, E.A.; et al. 2010 ACCF/AHA/AATS/ACR/ASA/SCA/SCAI/SIR/STS/SVM Guidelines for the Diagnosis and Management of Patients with Thoracic Aortic Disease. Circulation 2010, 121, e266–e369. [Google Scholar] [CrossRef]
  60. Yamanaka, K.; Tsuda, K.; Takahashi, D.; Washiyama, N.; Yamashita, K.; Shiiya, N. Bipolar Transesophageal Thoracic Spinal Cord Stimulation: A Novel Clinically Relevant Method for Motor-Evoked Potentials. JTCVS Tech. 2020, 4, 28–35. [Google Scholar] [CrossRef]
  61. Takahashi, S.; Orihashi, K.; Imai, K.; Mizukami, T.; Takasaki, T.; Sueda, T. Transintercostal-Evoked Spinal Cord Potential in Thoracic Aortic Surgery. Ann. Vasc. Surg. 2014, 28, 1775–1781. [Google Scholar] [CrossRef]
  62. Alqaim, M.; Cosar, E.; Crawford, A.S.; Robichaud, D.I.; Walz, J.M.; Schanzer, A.; Simons, J.P. Lumbar Drain Complications in Patients Undergoing Fenestrated or Branched Endovascular Aortic Aneurysm Repair: Development of an Institutional Protocol for Lumbar Drain Management. J. Vasc. Surg. 2020, 72, 1576–1583. [Google Scholar] [CrossRef] [PubMed]
  63. D’Oria, M.; Bertoglio, L.; Bignamini, A.A.; Mani, K.; Kölbel, T.; Oderich, G.; Chiesa, R.; Lepidi, S.; Abisi, S.; Adam, D.; et al. Editor’s Choice—PRINciples of Optimal antithrombotiC Therapy and Coagulation managEment during Elective Fenestrated and Branched EndovaScular Aortic repairS (PRINCE2SS): An International Expert Based Delphi Consensus Study. Eur. J. Vasc. Endovasc. Surg. 2022, 63, 838–850. [Google Scholar] [CrossRef] [PubMed]
  64. Kärkkäinen, J.M.; Cirillo-Penn, N.C.; Sen, I.; Tenorio, E.R.; Mauermann, W.J.; Gilkey, G.D.; Kaufmann, T.J.; Oderich, G.S. Cerebrospinal Fluid Drainage Complications during First Stage and Completion Fenestrated-Branched Endovascular Aortic Repair. J. Vasc. Surg. 2020, 71, 1109–1118.e2. [Google Scholar] [CrossRef] [PubMed]
  65. Borghese, O.; Brisard, L.; Le Corvec, T.; Hauguel, A.; Guimbretière, G.; Maurel, B. Spinal Cord Protection during Thoracic and Thoracoabdominal Endovascular Aortic Repair: 5-Year Results of a Preventive Protocol Including Prophylactic Cerebrospinal Fluid Drainage in High-Risk Patients. J. Endovasc. Ther. 2024, in press. [Google Scholar]
Jcm 12 07520 g001
Figure 1. Blood supply to the spinal cord.
Figure 1. Blood supply to the spinal cord.
Jcm 12 07520 g001
Jcm 12 07520 g002
Figure 2. Spinal cord injury following extensive coverage of lumbar and intercostal arteries and pre-existing occlusion of branches of the internal iliac artery.
Figure 2. Spinal cord injury following extensive coverage of lumbar and intercostal arteries and pre-existing occlusion of branches of the internal iliac artery.
Jcm 12 07520 g002
Jcm 12 07520 g003
Figure 3. Spinal cord injury due to thrombus embolism and pre-existing occlusion of the lumbar and intercostal arteries due to the shaggy aorta.
Figure 3. Spinal cord injury due to thrombus embolism and pre-existing occlusion of the lumbar and intercostal arteries due to the shaggy aorta.
Jcm 12 07520 g003
Jcm 12 07520 g004
Figure 4. Decisional algorithm for CSFD strategy.
Figure 4. Decisional algorithm for CSFD strategy.
Jcm 12 07520 g004
Table 1. Risk scoring for SCI adapted from Mousa et al. [25].
Table 1. Risk scoring for SCI adapted from Mousa et al. [25].
Age (by decade) 0.5
Celiac coverage1
Current smoker1
Dialysis1.5
3 or more aortic devices1
Emergent or urgent surgery1
Adjunct procedures aorta-related1.5
Adjunct procedures not aorta-related1.5
Total device length 19–31 cm1.5
Total device length ≥ 32 cm3
ASA class 4 or class 51
Total procedure time > 154 min1
High-volume center (tertiary referral center performing ≥ 50 procedures annually [26]) −1
eGFR > 60%−1
Estimated risk for spinal cord injuryTotal number of points
Low risk0–4
Medium risk4.5–6.5
High risk≥7
ASA, American Society of Anesthesiologists; eGFR, estimated glomerular filtration rate.
Table 2. Summary of key prevention strategies for spinal cord injury in complex endovascular repair of extent 1 to 3 thoracoabdominal aneurysms.
Table 2. Summary of key prevention strategies for spinal cord injury in complex endovascular repair of extent 1 to 3 thoracoabdominal aneurysms.
InterventionRationalPotential RisksEvidenceClass of Recommendations
Segmental artery occlusion for staged proceduresTriggers arterial collateralization and stabilizes blood supply to the spinal cord from alternate inflow sourcesExtended duration of treatment, risk of aneurysm rupture, spinal cord ischemiaCEACTS 2015: II-B
LSA revascularizationPreserves perfusion of vertebral arteryLaryngeal nerve injury, vocal cord paralysis, thoracic duct injuryPreventive
B–NR
B
C
C		ACC-AHA 2022: I
EACTS-ESVS 2019: II-A
ESVS 2017: II-A
EACTS 2015: II-A
Curative
C–LDACC-AHA 2022: II-B
Permissive hypertensionIncreases MAP to preserve blood flow in spinal cord collateral networkCardiac dysfunction, hemorrhageCEACTS 2015: II-A
High
hemoglobin threshold		Increases oxygen delivery to spinal cordTransfusion-associated complications, immunization, costCEACTS 2015: II-A
Perioperative neuromonitoringDetects early impaired spinal cord functionCost of medical devices, expertise required, false-positive rateC
C		ESVS 2017: II-B
EACTS 2015: II-B
Pharmacological adjunctsReduce spinal cord edema or excitatory amino acidsHyperglycemia, infection and gastrointestinal bleeding (steroids), postoperative pain (naloxone), hypovolemia (mannitol)CEACTS 2015: II-B
Selective CSFD drainageReduces CSFP and optimizes SCPPIntracranial and neuraxial bleeding, infection, mechanical complicationEarly
A
C
C
C		ACC-AHA 2022: I
ESVS 2017: II-A
EACTS 2015: II-A
ESC 2014: II-A
Delayed
C
C		EACTS-ESVS 2019: I
EACTS 2015: II-A
ACC-AHA 2022: Circulation, 2022;146:e334–e482 [35]. EACTS–ESVS 2019: Eur J Vasc Endovasc Surg (2019) 57, 165e198 [36]. ESVS 2017: Eur J Vasc. Endovasc Surg (2017) 53, 4e52 [37]. EACTS 2015: European Journal of Cardio-Thoracic Surgery 47 (2015) 943–957 [24]. ESC 2014: European Heart Journal (2014) 35, 2873–2926 [38].
Table 3. Secondary spinal cord injuries.
Table 3. Secondary spinal cord injuries.
Extra-Neurologic (Systemic)Neurologic
HypoxemiaSpinal cord compression (hematoma, tumor)
Low blood pressure Vasospasm
HypercapniaSeizure
AnemiaInfection
Hyperthermia
Hyperglycemia
Hypocapnia
Hyponatremia/Hypernatremia
Table 4. Listing of major risk factors for spinal cord ischemia (adapted from Nantes university hospital protocol [64]).
Table 4. Listing of major risk factors for spinal cord ischemia (adapted from Nantes university hospital protocol [64]).
Total aortic coverage > 200 mm
Coverage of the area Th9–Th12
Supra-celiac coverage > 40 mm
LSA or hypogastric coverage without immediate revascularization strategy
Prior aortic repair (abdominal and/or thoracic descending—endovascular and/or open surgery)
Prior spinal cord injury episode during TEVAR procedure or recent AAS (<15 days)
Procedure in the first 15 days following AAS
AAS, acute aortic syndrome; LSA: left subclavian artery.
Disclaimer/Publisher’s Note: The statements, opinions and data contained in all publications are solely those of the individual author(s) and contributor(s) and not of MDPI and/or the editor(s). MDPI and/or the editor(s) disclaim responsibility for any injury to people or property resulting from any ideas, methods, instructions or products referred to in the content.

Share and Cite

MDPI and ACS Style

Brisard, L.; El Batti, S.; Borghese, O.; Maurel, B. Risk Factors for Spinal Cord Injury during Endovascular Repair of Thoracoabdominal Aneurysm: Review of the Literature and Proposal of a Prognostic Score. J. Clin. Med. 2023, 12, 7520. https://doi.org/10.3390/jcm12247520

AMA Style

Brisard L, El Batti S, Borghese O, Maurel B. Risk Factors for Spinal Cord Injury during Endovascular Repair of Thoracoabdominal Aneurysm: Review of the Literature and Proposal of a Prognostic Score. Journal of Clinical Medicine. 2023; 12(24):7520. https://doi.org/10.3390/jcm12247520

Chicago/Turabian Style

Brisard, Laurent, Salma El Batti, Ottavia Borghese, and Blandine Maurel. 2023. "Risk Factors for Spinal Cord Injury during Endovascular Repair of Thoracoabdominal Aneurysm: Review of the Literature and Proposal of a Prognostic Score" Journal of Clinical Medicine 12, no. 24: 7520. https://doi.org/10.3390/jcm12247520

Note that from the first issue of 2016, this journal uses article numbers instead of page numbers. See further details here.

Article Metrics

Back to TopTop