Ann Thorac Surg 2007;83:1345-1355
© 2007 The Society of Thoracic Surgeons
Original Articles: Cardiovascular
Delayed Spinal Cord Deficits After Thoracoabdominal Aortic Aneurysm Repair
Daniel R. Wong, MD, MPHa,b,
Joseph S. Coselli, MDa,b,
Karen Amerman, MS, CRNAa,b,
John Bozinovski, MDa,b,
Stacey A. Carter, BAa,b,
William K. Vaughn, PhDa,
Scott A. LeMaire, MDa,b,*
a Texas Heart Institute at St. Luke’s Episcopal Hospital, Houston, Texas
b Division of Cardiothoracic Surgery, Baylor College of Medicine, Houston, Texas
Accepted for publication November 9, 2006.
* Address correspondence to Dr LeMaire, Baylor College of Medicine, One Baylor Plaza, BCM 390, Houston, TX 77030 (Email: slemaire{at}bcm.edu).
Presented at the Fifty-second Annual Meeting of the Southern Thoracic Surgical Association, Orlando, FL, Nov 10–12, 2005.
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Abstract
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Background: Limited information is available about the treatment and outcomes of delayed paraplegia after thoracoabdominal aortic aneurysm (TAAA) repair. The objective of this study was to assess factors that precipitate and favorably affect delayed-onset neurologic deficits.
Methods: Over a 19-year period, 2,368 TAAA repairs were performed. Of the 93 patients (3.9%) who had postoperative paraplegia or paraparesis, 34 (37%) initially had intact neurologic function, but a delayed spinal cord deficit developed. We retrospectively examined clinical factors and events associated with development of the deficits, treatments used, and outcomes. Factors related to functional status were evaluated by comparing survivors who were ambulatory at discharge or transfer with those who were not.
Results: The delayed deficits occurred between 13 hours and 91 days postoperatively and were associated with a period of hypotension in 9 patients (26%). Two patients (6%) died in hospital. Of the 32 patients discharged or transferred, 13 (41%) were ambulatory. Poor functional outcomes were associated with female sex, intraoperative cerebrospinal fluid drainage, fewer intercostal arteries reattached, and administration of corticosteroids or osmotic diuretics. The actuarial survival rate at 2 years was 80% ± 13% for the ambulatory patients and 32% ± 12% for the nonambulatory patients (p = 0.002).
Conclusions: Although precipitating episodes of hypoperfusion were common, most cases of delayed paraplegia occurred without such events, suggesting that other factors may play an important role in the development of this complication. Ambulatory status at discharge significantly predicts midterm survival.
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Introduction
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Paraplegia and paraparesis are devastating complications of thoracic aortic surgery. Thoracoabdominal aortic aneurysm (TAAA) repair may jeopardize the supply of blood to the spinal cord in patients whose collateral blood supply may already be tenuous. A number of intraoperative management strategies have been implemented to reduce spinal cord ischemia. These strategies—including the use of left heart bypass, reattachment of segmental intercostal and lumbar arteries, and cerebrospinal fluid (CSF) drainage [1–4]—appear to be particularly helpful in reducing the risk of immediate-onset postoperative neurologic deficits. In contrast to immediate spinal cord deficits, the topic of delayed neurologic injury has garnered little attention in the surgical literature and remains poorly understood [5–8]. A variety of therapeutic interventions have been implemented with variable success in reversing delayed neurologic deficits [9]. The impact of these treatment strategies on outcome, however, has not been elucidated. For this reason, we reviewed our 19-year experience with TAAA repair to evaluate factors that may precipitate delayed-onset paraplegia and paraparesis, the efficacy of therapeutic interventions, and survival and functional outcomes, specifically ambulatory status at hospital discharge or transfer.
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Patients and Methods
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Patients
Institutional Review Board approval was obtained for this study and for waiver of individual consent. Since 1986, 2,368 consecutive TAAA repairs have been performed by the service of the senior surgeon (J.S.C.). Based on perioperative data from a prospectively maintained database, postoperative paraplegia or paraparesis developed in 93 patients (3.9%), 34 (37%) of whom awoke from general anesthesia with intact neurologic function and subsequently had a new spinal cord deficit; this group with delayed-onset deficits is the focus of this report. Records were reviewed to determine (1) patients’ clinical characteristics and operative details, (2) events associated with development of the deficits, (3) treatments used in an attempt to reverse the deficits, and (4) outcomes.
Surgical Techniques
Our approach to the management of TAAAs has been thoroughly described elsewhere [10, 11]. To prevent spinal cord ischemia, we routinely used moderate systemic heparinization (1.0 mg/kg) and mild permissive hypothermia (32°C to 34°C, nasopharyngeal). Significant segmental intercostal or lumbar arteries (T8 to L1) were consistently reattached [12]. Cerebrospinal fluid drainage and left heart bypass have become frequent adjuncts during more extensive TAAA repairs (Crawford extents I and II) [5]. Left heart bypass was conducted by using a closed circuit with a centrifugal pump; inflow was established through a left atrial cannula, and blood was returned through a cannula in the distal descending thoracic aorta or left femoral artery. We did not use total cardiopulmonary bypass with hypothermic circulatory arrest unless the aortic arch was aneurysmal and required resection or proximal aortic cross-clamping was not technically feasible. Evoked potential monitoring was not used.
Perioperative Variables
Chronic renal insufficiency was indicated by a serum creatinine value exceeding 2 mg/dL. Coronary artery disease was defined as documented coronary stenosis greater than 50% or a history of angina, myocardial infarction, or coronary angioplasty or bypass. Chronic medical therapy for hypertension or diabetes mellitus was considered an indicator of these diseases. A positive smoking history was recorded for patients who had used any form of tobacco in the past.
A presentation was considered acute if accompanied by acute pain, rupture, contained rupture, or complicated acute dissection [13]. Aortic dissection was considered acute if surgery was performed within 14 days after the onset of pain and chronic if surgery was performed 15 or more days after the onset. Patients were considered symptomatic if they had any symptom (acute or chronic, severe or mild) relating to the aneurysm, including pain, hoarseness, or dysphagia. Surgical procedures were considered emergent if immediate surgery was required because of an acute life-threatening condition, urgent if surgery was required during the same hospitalization because of deterioration in clinical status, and elective if the patient’s TAAA was stable before surgery and the procedure could be delayed without serious risk.
The extent of the aneurysm repair was described according to the original Crawford classification system [5]. Aortic clamp and intercostal ischemic times were collected. Unprotected ischemic time was defined as the duration of ischemia during which the patient was not supported by concomitant left heart bypass.
Delayed-Onset Deficits
Delayed spinal cord deficits included weakness (paraparesis) and flaccid paralysis (paraplegia). Potential precipitating events were defined as acute changes in clinical status that were temporally related to the development of the deficits; the nature of the precipitant was documented. The severity of the motor deficit at onset was graded on a 0 to 5 scale as follows: 0 = total paralysis of all limb muscles; 1 = palpable or visible contraction; 2 = no active movement with gravity; 3 = active movement against gravity only; 4 = active movement against some resistance; 5 = active movement against full resistance. Bladder dysfunction was defined as the need for indwelling or intermittent catheterization to adequately empty the bladder, or urinary incontinence in the absence of other urinary tract pathology. Bowel dysfunction was defined as the inability to control defecation, manifested as fecal incontinence or obstipation.
Treatment of Delayed-Onset Deficits
We examined the frequency with which each of the following therapeutic maneuvers was used: the administration of pharmacologic agents, including vasopressors, systemic corticosteroids, naloxone, and osmotic agents (eg, mannitol, glycerol); blood transfusion; and CSF drainage.
Outcomes
Operative mortality was defined as death within 30 days of operation or during the initial hospitalization. Hospital-to-hospital transfer was not considered a discharge, and deaths that occurred after such a transfer were counted as operative deaths. Transfer to a nursing home or rehabilitation center was considered a discharge unless the death was due to a complication directly related to the operation. The severity of lower-limb weakness was recorded 24 hours after the onset of the deficit and at the time of discharge or transfer. On the basis of functional status at discharge or transfer, survivors were classified as either ambulatory (walking independently or with a walker) or nonambulatory (requiring a wheelchair). Medium- and long-term survival were assessed through direct contact with the patient, a family member, or the primary physician, or by searching the Social Security Death Index database. Follow-up information was available for all patients; the mean follow-up time was 2.4 ± 3.5 years (range, 4 days to 17 years) after operation.
Statistical Analysis
Two comparisons of variables were performed: patients who were ambulatory at discharge or transfer were compared with those who were not, and the 34 patients with delayed deficits were compared with the 59 patients with immediate deficits. Statistical analysis was conducted with SAS software (SAS Institute, Cary, North Carolina). The 
2 and Fisher’s exact test were used to compare discrete variables, and the Wilcoxon rank sum test was used for continuous variables. Kaplan-Meier probability curves were constructed and compared by using the log-rank test. The multivariable logistic regression that was performed to find independent predictors of ambulatory status at discharge was limited by the small number of patients with deficits, which precluded stable modeling of more than one variable in the model (hence, univariate statistics sufficed and were reported). No correction for multiple testing was made.
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Results
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Clinical Characteristics
Table 1
lists the preoperative characteristics and intraoperative details for the 34 patients who had delayed-onset deficits. Most patients had degenerative aneurysms without dissection. Seven patients presented acutely, but none had ruptured aneurysms or required emergent surgery. The majority underwent extent II repairs. Segmental intercostal or lumbar arteries were reattached in 24 patients (71%). Left heart bypass was used in 12 patients (35%), and CSF drainage was used intraoperatively in 15 (44%).
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Table 1 Preoperative Characteristics and Operative Details of 34 Patients Who Had Delayed-Onset Paraplegia or Paraparesis After Thoracoabdominal Aortic Aneurysm Repair
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Delayed-Onset Deficits
The onset of delayed paraplegia and paraparesis occurred 13 hours to 91 days postoperatively (mean, 6.2 ± 15.7 days; median, 3 days) and was associated with an episode of hypotension in 9 patients (26%). Of these, 2 experienced multisystem organ failure from sepsis or bowel ischemia. Another patient had sepsis syndrome with concomitant hypotension. Atrial fibrillation with rapid ventricular response was the precipitant in 2 patients. Two other patients experienced transient hypotension during acute respiratory decompensation requiring intubation. In 1 patient, hypotension developed with a hemothorax requiring tube thoracostomy but no surgical intervention. One patient had refractory hypotension of unknown cause.
Twenty-six patients (76%) had symptoms of neurologic injury while still in the intensive care unit. In all cases, the deficit was bilateral. Nineteen patients (56%) had paraplegia (motor score of 0). Associated bladder dysfunction occurred in 15 patients (44%), and 9 (26%) had bowel dysfunction.
Treatment of Delayed-Onset Deficits
The treatments initiated upon diagnosis of delayed-onset paraplegia are listed in Table 2. Corticosteroids and mannitol were the most commonly used medications. Seven patients (21%) received vasopressor agents to raise spinal perfusion pressure. Cerebrospinal fluid drainage was used in 23 patients (68%).
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Table 2 Therapeutic Maneuvers Used to Treat Delayed-Onset Paraplegia or Paraparesis After Thoracoabdominal Aortic Aneurysm Repair in 34 Patients
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Outcomes
There were 2 in-hospital deaths. One death resulted from postoperative sepsis that culminated in disseminated intravascular coagulopathy and multiorgan failure. The other death was due to postoperative bowel ischemia and multiorgan failure. Of the 32 patients who survived to discharge or transfer, 13 patients (41%) were ambulatory (3 walking independently and 10 with use of a walker), and 19 patients (59%) were nonambulatory.
A noteworthy patient in this series was a 60-year-old man with coronary artery disease, hypertension, and previous ascending aortic repair. He underwent a Crawford extent II TAAA repair with reattachment of two pairs of intercostal arteries, intraoperative CSF drainage, and left heart bypass. Ninety-one days postoperatively, hypotension developed while the patient was being treated for sepsis, and he became abruptly paraparetic (leg strength, 1/5 bilaterally). Twenty-four hours after the onset of his deficit, his leg strength had not improved; however, at hospital discharge 39 days later, his left leg strength was 3/5 and right leg strength was 5/5. He was walking independently at discharge and continues to do so with a cane 5 years postoperatively.
Surviving patients who were ambulatory at the time of discharge or transfer differed in several ways from those who were not (Table 3). Ambulatory patients were more often male, with trends toward younger age, dissections, and absence of chronic hypertension and diabetes; more intercostal arteries were reattached, and they incurred longer unprotected aortic cross-clamp times. Poor functional outcomes were associated with intraoperative CSF drainage and with the use of corticosteroids, osmotic diuresis, or both. There was a trend toward nonambulatory status among patients treated with vasopressors, including those administered in combination with other therapies. No patients with paraplegia at the time of deficit onset, or at 24 hours after the event, were ambulatory at discharge or transfer.
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Table 3 Characteristics of Ambulatory Versus Nonambulatory Patients With Delayed-Onset Neurologic Deficits After Thoracoabdominal Aortic Aneurysm Repair
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Follow-up data were available for all 34 patients. Overall actuarial survival was 47% ± 10% at 2 years and 31% ± 10% at 5 years. Two-year survival was 80% ± 13% for the ambulatory group and 32% ± 12% for the nonambulatory group (p = 0.002; Fig 1).
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Fig 1. Survival of ambulatory and nonambulatory patients with delayed neurologic deficit after thoracoabdominal aortic aneurysm repair. The numbers at risk (small font below) are given. The curves are truncated at 3 years because of the small numbers at risk beyond this point.
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Comparison With Immediate-Onset Deficits
There were several differences between the delayed-onset deficit patients and the 59 immediate-onset deficit patients (Table 4). The immediate-onset group included 22 emergent patients (37%), 13 of whom had ruptured aneurysms (22%); in contrast, there were no ruptured aneurysms in the delayed-onset group. The immediate group had longer unprotected intercostal ischemic time and unprotected aortic clamp time, although extent of repair was similar between the two groups. Although the severity of the deficit at its onset was no different, the immediate-onset group had significantly more bowel and bladder dysfunction and had less need for reinsertion or primary insertion of CSF drains. Immediate deficits were more common in the early portion of the study period.
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Table 4 Characteristics of Patients With Delayed- Versus Immediate-Onset Deficit After Thoracoabdominal Aortic Aneurysm Repair
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Overall survival was not significantly different between these two groups; 5-year survival was 31% in both (Fig 2). Within the immediate-onset group, survival was unrelated to ambulatory status among those surviving to hospital discharge (Fig 3).
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Fig 2. Survival of patients with delayed and immediate neurologic deficit after thoracoabdominal aortic aneurysm repair. The numbers at risk (small font below) are given with the curves truncated at 5 years.
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Fig 3. Survival of ambulatory and nonambulatory patients with immediate neurologic deficit after thoracoabdominal aortic aneurysm repair. The numbers at risk (small font below) are given with the curves truncated at 5 years.
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Comment
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Postoperative paraplegia and paraparesis are devastating complications of TAAA repair. Patients who experience them have not only the incumbent physical disability but also a higher mortality rate [14]. Repair of TAAA is unique in that a large number of segmental intercostal and lumbar arteries providing spinal cord perfusion may be disrupted, especially in patients with more extensive aneurysms. The determining factors for ischemic spinal cord injury include the duration of ischemia, the metabolic rate of the spinal cord, and the degree of reperfusion injury that occurs when blood flow is reestablished. The presence of paraplegia immediately upon emergence from anesthesia suggests that there has been an irreversible ischemic injury to the spinal cord, perhaps related to interruption of its vascular supply. In contrast, initially normal neurologic findings suggest that the vascular supply to the spinal cord was intact after the operation. Delayed-onset deficits, therefore, probably result from a state of malperfusion that may be reversible with appropriate therapeutic intervention.
The reported incidence of ischemic spinal cord injury varies widely, from 0% to 40% [2, 9, 15–21]. Table 5
lists the immediate and delayed deficit rates from several recent series. To reduce the rate of these deficits, various techniques have been advocated to optimize spinal cord blood flow. Intraoperative modalities include distal aortic perfusion, reattachment of critical intercostal or lumbar arteries, CSF drainage, and monitoring of somatosensory- or motor-evoked potentials [1, 2, 4, 21–23]. Postoperative strategies for optimizing spinal cord perfusion include maintaining an adequate systemic blood pressure and continuing CSF drainage. Despite these measures, however, deficits still occur and are influenced by such factors as the presence of acute dissection, extent of repair, aortic clamp time, and previous aortic surgery [13]. Some authors have suggested that the relative frequency of delayed deficits has increased with the increasing use of more aggressive spinal cord protection measures in the perioperative period [9, 21].
Specific risk factors for this type of deficit have not been identified, other than postoperative hypotension leading to spinal cord malperfusion [24, 25]. It is also known that more extensive TAAA repairs (ie, Crawford extent II) result in higher paraplegia rates [7, 18, 26–28]. Crawford extent II TAAA repairs accounted for 50% of the patients with delayed deficits in our series. It is noteworthy that 16 of our 17 patients with extent II repairs had at least one pair of segmental arteries reattached.
Although the female patients in our series tended to have a poorer ambulatory status, other studies have not identified female sex as a risk factor for delayed paraplegia, nor have they examined the impact of sex on ambulation [21, 24]. Furthermore, in our series, functional outcomes were unaffected by the presence of coronary artery disease, renal insufficiency, previous smoking history, previous aneurysm repair, aneurysm rupture, or the acuity of presentation. A trend towards worse ambulatory status was seen in patients with hypertension and diabetes. It has been well documented that complete or partial recovery of neurologic function can be attained with appropriate interventions, which may be more critical than these preoperative risk factors.
Regarding operative variables, patients with a greater number of intercostal arteries reattached were more likely to ambulate at discharge. Safi and colleagues [4] determined that a lack of segmental arterial reattachment at various thoracolumbar levels resulted in specific early or delayed deficits. Jacobs and associates [23] used motor evoked potential changes to indirectly evaluate segmental spinal cord blood supply; they contend that a diffuse collateral network provides spinal cord blood supply in those with degenerative TAAAs. Our study suggests that reattaching a greater number of segmental arteries increases the likelihood of maintaining this rich collateral network, thereby potentially reducing the severity of delayed deficits.
The postoperative precipitating factors for neurologic deficit and the treatment of these precipitants are the focus of much of the recent literature [9, 21, 24]. Azizzadeh and coworkers [24] found that postoperative mean arterial pressure <60 mm Hg and CSF drain complications predicted delayed deficits. Although postoperative hypotension was an important precipitating event in our series, none of our patients had an identifiable inciting CSF drain complication. Estrera and colleagues [18] noted that perioperative adjuncts were associated with risk of delayed neurologic deficit; they suggested that a previously vulnerable spinal cord blood supply may be protected with adjunctive measures but remain vulnerable to delayed deficit once these measures are withdrawn postoperatively. In our study, hypotension was associated with some, but not all, delayed-onset deficits. Other factors may have been important, including rheologic and thrombotic factors.
In this observational study, the association of various treatments, such as corticosteroids, with worse outcomes was probably confounded, because the most aggressive interventions were applied in the most severely affected patients. Without randomized trials, it is difficult to determine the real effect of these measures. This treatment bias is evident in the finding that less severe deficits (paraparesis initially and at 24 hours) were associated with better ambulation. Not surprisingly, 2-year survival also was significantly better in the ambulatory group, with no survivors in the nonambulatory group beyond approximately 5 years. This finding supports the contention by Svensson and coworkers [14] that paraplegia limits survival. We were unable, however, to document any association between survival and ambulatory status in patients with immediate-onset paraplegia.
Multimodality Approach to Preventing and Treating Delayed-Onset Paraplegia
We advocate a multimodality approach to organ protection for repair of TAAAs, with preoperative assessment and optimization of physiologic reserve, and with individualized tailoring of the operative strategy [3]. Intraoperative strategies include moderate heparinization (1 mg/kg); permissive mild hypothermia (32°C to 34°C, nasopharyngeal); aggressive reattachment of segmental arteries, especially from T8 to L1; renal artery perfusion with 4°C crystalloid solution if feasible; and sequential aortic clamping if feasible. For Crawford extent I and II thoracoabdominal repairs, we use CSF drainage (drained to gravity to maintain CSF pressure of 10 to 12 mm Hg), left heart bypass during the proximal anastomosis, and selective perfusion of the celiac axis and the superior mesenteric artery during the intercostal, visceral, and renal anastomoses [3].
Postoperatively, CSF pressures are monitored for approximately 48 hours; unless there are neurologic signs or symptoms, CSF is drained as much as 10 cc/h to maintain a pressure of 12 to 15 mm Hg. Euglycemia is maintained with an insulin infusion protocol. Anemia, atrial dysrhythmias, respiratory distress, and hypotension are treated aggressively. The timely correction of underlying physiologic aberrations and aggressive management of blood pressure is crucial.
With the onset of a new neurologic deficit, we recommend monitoring the patient in a critical care setting, aiming to achieve a mean arterial blood pressure of at least 90 mm Hg by using appropriate agents and by draining CSF to a pressure of 8 to 10 mm Hg. A new CSF drain is inserted if not already present. Currently, it is our practice to administer systemic corticosteroids and mannitol for 48 hours. Patients with hyperthermia in excess of 37.8°C receive acetaminophen; additional measures, such as passive or active cooling (ie, cooling blanket), are used when temperatures exceed 38.3°C. The metabolic requirements of neural tissue are elevated with hyperthermia, and the production of free radicals and release of stress-related proteins may amplify the effects of ischemia on the spinal cord.
Limitations
This study had a few noteworthy limitations. Although we examined a large number of TAAA repairs, the infrequency of delayed-onset deficits limited the power of our study. Significant changes in the treatment of these patients occurred during the study period, whose 19-year length was necessary to achieving a useful sample size. It is difficult to know how these changes in treatment approach may have affected clinical outcomes during different portions of this long study period. As awareness of delayed neurologic deficits has increased, rigorous efforts have been undertaken to educate surgical house staff and nursing staff in the early identification and management of such deficits.
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Discussion
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DR THORALF SUNDT (Rochester, MN): Joe, a beautifully presented paper that can only be criticized for its conspicuous lack of potential Tiki Award candidates. This is great that you have highlighted the importance of delayed paraplegia. It is important for the audience to note that 25% of the paraplegia that you saw was delayed. So in your practice this phenominon now represents a significant percentage of the paraplegia that you are seeing.
The only way I can think of to battle this problem is reimplanting more intercostals. This brings to mind the discussion you and I have had before: you are there to take aorta out, not leave aorta in. How has the recognition of the importance of this problem changed your approach to how many intercostals you leave in? What are the implications for stent grafting, which will obviously cover all of these intercostals? Do you have any other practical pointers for us?
DR COSELLI: Thank you very much. Although it is subtle and we haven’t had a chance to evaluate it thoroughly, I would have to say that personally it probably has leaned me toward—because the one thing that was significant is reattachment of intercostals and, by implication, lumbar arteries—being more aggressive in that area. This is frequently difficult in the acute setting where there is a rupture in the area that you are interested in trying to reattach. Interestingly, Panneton, in a meta-analysis of the literature from about 10 years ago, showed that paraplegia was delayed in 30% of cases in the literature of thoracoabdominals up to that point; this really hasn’t changed significantly since then.
Patient selection is important. If a patient has either immediate or delayed paraplegia, in order to be somewhat ambulatory, with a walker or cane, it requires upper body strength, and that is where age and other factors, as I mentioned, come in, and that implicates important aspects of whether or not a patient is actually going to survive over the short and midterm.
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Acknowledgments
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The authors wish to thank Virginia Fairchild and Stephen N. Palmer, PhD, ELS, for editorial assistance and Garry Borsato, MD, for assistance with data collection.
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References
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C. D. Etz, M. Luehr, F. A. Kari, C. A. Bodian, D. Smego, K. A. Plestis, and R. B. Griepp
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J. Thorac. Cardiovasc. Surg.,
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Abstract
Introduction
