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J Thorac Cardiovasc Surg 2008;135:324-330
© 2008 The American Association for Thoracic Surgery
Surgery for Acquired Cardiovascular Disease |
a Department of Cardiothoracic Surgery, Mount Sinai School of Medicine, New York, NY
b Department of Anesthesiology, Mount Sinai School of Medicine, New York, NY
c Department of Thoracic and Cardiovascular Surgery, University Hospital of Münster, Münster, Germany
Received for publication June 24, 2007; revisions received October 25, 2007; accepted for publication November 1, 2007. * Address for reprints: Christian D. Etz, MD, Mount Sinai School of Medicine, Department of Cardiothoracic Surgery, One Gustave L. Levy Place, PO Box 1028, New York, NY 10029. (Email: christian.etz{at}mountsinai.org).
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Abstract |
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Methods: A series of 858 thoracoabdominal aneurysm repairs (June 1990–June 2006) with an overall paraplegia rate of 2.7% was analyzed retrospectively. Serial segmental artery sacrifice was monitored by using somatosensory evoked potentials; segmental arteries were not reimplanted. Of a total of 20 cases of paraplegia, 3 occurred intraoperatively and 7 occurred late postoperatively: these will not be analyzed further. In 10 cases (the paraplegia group) spinal cord injury occurred within 48 hours after thoracoabdominal aneurysm repair, despite intact somatosensory evoked potentials at the end of the procedure. These patients with early postoperative delayed paraplegia were compared with 10 matched control subjects who recovered without spinal cord injury.
Results: In the paraplegia group a median of 9 segmental arteries (range, 5–12 segmental arteries) were sacrificed. There were 9 male subjects: median age was 63 years (range, 40–79 years), and 4 of 10 had cerebrospinal fluid drainage. A median of 9 segmental arteries (range, 2–12 segmental arteries) were also sacrificed in the matched recovery group. There were 4 male subjects; median age was 66 years (range, 40–78 years), and 8 of 10 had cerebrospinal fluid drainage. During the first 48 hours postoperatively, there were no significant differences in arterial and mixed venous oxygen saturation, partial arterial O2 and CO2 pressures, body temperature, glucose, hematocrit, or pH. The mean central venous pressures, however, were significantly higher in the paraplegic patients from 1 to 5 hours postoperatively (P = .03). In addition, although absolute mean aortic pressures did not differ between matched pairs postoperatively, when pressures were considered as a percentage of individual antecedent preoperative mean aortic pressure, paraplegic patients had significantly lower values during the first 5 hours postoperatively (P = .03).
Conclusions: This study suggests that paraplegia can result from inadequate postoperative spinal cord perfusion caused by relatively minor differences from control subjects in perfusion parameters. Delayed paraplegia can perhaps be prevented with better hemodynamic and fluid management.
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Introduction |
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A number of adjuncts have been successfully used to counteract the consequences both of spinal cord ischemia during surgical intervention and a precarious spinal cord blood supply postoperatively, and the incidence of paraplegia and paraparesis at centers for aneurysm repair has been decreasing.4-12 However, the occasional case of spinal cord injury still occurs, and it remains unclear which factors are most important in preventing either immediate or delayed paraplegia.
Recent clinical and experimental studies suggest that ischemic spinal cord injury is not inevitable, even with extensive segmental artery (SA) sacrifice.13-15 With the aid of intraoperative electrophysiologic monitoring, it has become apparent that some patients do not sustain any spinal cord injury intraoperatively with extensive sacrifice of intercostal and lumbar arteries but nevertheless have paraplegia either immediately postoperatively or even weeks after the operation. This so-called delayed-onset paraplegia accounts for up to one third of cases of postoperative permanent spinal cord injury16,17 and in recent experience constitutes the majority of patients with spinal cord injury at our institution.
The current retrospective study concerns 10 cases of paraplegia that developed within 48 hours after surgical intervention despite intact somatosensory evoked potentials (SSEPs) throughout the operation. In this study the patients with paraplegia are compared with 10 matched control patients operated on contemporaneously who recovered spinal cord function. All available intraoperative and postoperative physiologic measurements that might have had an influence on spinal cord function were compared between affected patients and their matched control subjects to try to pinpoint factors that might have contributed to the development of this early, postoperative, delayed-onset spinal cord injury.
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Materials and Methods |
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The overall hospital mortality in the entire series of patients (including emergencies and reoperations) was 9.7%.
Paraplegia Group
This report focuses on 10 cases of delayed-onset permanent paraplegia in which spinal cord injury occurred within 48 hours after TAA/A repair involving SA sacrifice, despite intact SSEPs at the end of the procedure: these are designated the paraplegia group, and their clinical characteristics are outlined in
Table 1. These cases of early postoperative paraplegia despite intact SSEPs intraoperatively represent the largest subgroup among cases of paraplegia or paraparesis at our institution since the introduction of SSEP monitoring.18
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Figure 1. Although SSEP monitoring was not introduced until 1993 (or motor evoked potential [MEP] monitoring until 2002), the operative strategy and postoperative management of all the patients in this series was otherwise the same. We designated 3 patients with severe intraoperative ischemia with SSEP loss as having experienced immediate postoperative paraplegia. One of these recovered spinal cord function postoperatively. In addition to the 10 patients with early delayed paraplegia, there were 7 patients who had onset of spinal cord injury several days to several weeks after the procedure. Five of these patients had paraplegia (one after cardiopulmonary resuscitation and another after a laparotomy), and 2 were left with paraparesis. No patient had paraplegia more than 3 weeks after SA sacrifice during TAA/A repair. Neither the patients with intraoperative nor those with late delayed-onset paraplegia will be considered further.
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Figure 2] by using the same surgical technique) were selected. The control subjects, designated the recovery group, were chosen by taking the individuals who had undergone roughly equivalent operations closest in time to the paraplegic patients but had survived with intact spinal cord function. The postoperative parameters analyzed were not included in the database from which the patients were selected and therefore could not have influenced the choice of control subjects. Patient characteristics in the recovery group are also shown in Table 1.
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The most common indication for TAA/A replacement (Table 1) was an atherosclerotic aortic aneurysm, which was noted in 7 of the paraplegic patients and 8 of the control subjects; a chronic dissection, however, was present in 4 of the patients in the paraplegia group and 1 of the control subjects. One patient in the paraplegia group had Marfan syndrome.
As might have been anticipated, hypertension was present in most of the patients in both groups: 8 in the control group and 7 in the paraplegia group. There was a comparable incidence of history of coronary artery disease (P = 1.0). Of factors thought to be associated with a generally less favorable outcome, age was marginally higher in the recovery group, which also contained more female patients, slightly more patients with diabetes, and more patients with previous abdominal aneurysm operations. Several other risk factors, however, were more prevalent in the paraplegia group: a higher proportion of smokers and patients with chronic obstructive pulmonary disease and situations requiring urgent and emergency operations.
Among intraoperative factors, the diameter of the aneurysm was the same in both the paraplegia and recovery groups, as was the extent of the aneurysm, reflected by the number of SAs that were sacrificed (Figure 2). The patients in the paraplegia group, however, had a somewhat higher incidence of intraluminal clot and of contained rupture.
Operative Management
All patients are placed in the standard thoracoabdominal position. A double-lumen endotracheal tube is used to isolate the left lung. A right radial arterial line, a right common femoral line, and a pulmonary artery catheter are inserted. Intraoperative transesophageal echocardiography is used in all patients. Since 1990, a spinal catheter has been placed whenever possible, and cerebrospinal fluid (CSF) pressure has been monitored during the operation and for the subsequent 72 hours: the CSF is drained at a maximum rate of 15 mL/h, as long as the CSF pressure remains greater than 10 mm Hg. Since 1993, SSEP monitoring has been used intraoperatively, with the addition of MEP monitoring since 2002. SSEP monitoring is continued for the first 12 hours postoperatively.4,19
Operative Technique
The essential steps of our approach to the repair of descending TAA/As have been described previously. The aorta is accessed through a left thoracotomy or thoracoabdominal incision. The diaphragm is divided circumferentially. The infradiaphragmatic aorta is exposed through a retroperitoneal approach. Once the aneurysm has been fully exposed, the SAs are serially temporarily occluded, and if no change in the MEPs or SSEPs occurs, each one is subsequently ligated before the aneurysm is removed. All operations are carried out under moderate hypothermia (32°C). If needed, deep hypothermia is used, with circulatory arrest initiated at a bladder temperature of 15°C and a jugular bulb cerebral venous saturation of 95% or greater.
Postoperative Management
Aggressive fluid administration for at least the first 24 postoperative hours is initiated, aiming for a mean aortic pressure of 80 to 90 mm Hg, with peripheral vasoconstrictors administered as necessary to maintain this pressure. Gentle diuresis is begun 48 to 72 hours after the operation. SSEPs, when used, are monitored until the patient awakens. Thereafter, hourly brief neurologic examinations are performed for 72 hours. CSF drainage (as previously described) is continued for 72 hours. Steroids are tapered over 48 to 72 hours.
Statistical Methods
All statistical analyses of these data were based on methods for matched pairs, although for the purpose of clinical interest, some outcomes are described as overall medians, means, or percentages for the paraplegic patients and the recovered control subjects. McNemar tests with exact P values were used for comparing categorical data. Wilcoxon signed-rank tests were used to compare continuous characteristics. The first 5 hourly repeated measures were compared in a random-effects mixed model. A similar model was used for comparing the patients and control subjects in terms of the average of their nonmissing measurements during the first 5 hours, hours 6 to 24, and hours 25 to 48.
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Results: Comparability of Experimental Groups |
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Tests of case-control differences among 10 paraplegic patients and their matched nonparaplegic control subjects (McNemar tests with exact P values) revealed a slight preponderance of male subjects (p = .125) in the paraplegia group, as well as a history of smoking (P = .375), as shown in Table 1. Multiple other factors were also tested, but with the small numbers involved, there was no chance of finding significance because cases and control subjects were the same in 7 or more pairs: this was true of the presence of diabetes and chronic obstructive pulmonary disease.
Intraoperatively, the most important finding was that all the patients had intact SSEPs throughout the procedure. There were, however, as noted above, more patients in the paraplegia group with emergency or urgent procedures, clot noted during the course of the operation (P = .38), and contained rupture (P = .69). Although the mean temperatures were the same in both groups, there were more patients who underwent operations with deep hypothermic circulatory arrest in the recovery group.
During the first 48 hours postoperatively, there were no significant differences in mean arterial O2 saturation, arterial partial O2 and CO2 pressures, body temperature during rewarming, glucose levels, hematocrit values, and pH. Mixed venous saturation, which was used to detect variability in cardiac output during the postoperative period, also did not significantly differ between the pairs in the paraplegia and recovery groups (
Table 2).
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Figure 3), however, were significantly higher in the paraplegic patients from 1 through 5 hours postoperatively (overall P = .03); the most marked differences occurred at 2, 3, and 4 hours (P = .02, P < .005, and P = .03, respectively). Of note (see the Discussion section), 4 of 10 of the group with subsequent paraplegia had CSF drainage, in contrast with 8 of 10 patients who had recovery of function (P = .125, Table 1).
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Figure 4, A), if the pressures were considered in relation to each patient's antecedent baseline arterial pressure, which was obtained after placement of the arterial line at hospital admission or before surgical intervention, then the arterial pressures in the paraplegic patients were significantly less than those in the control group during the first 5 hours postoperatively (P = .027; Figure 4, B).
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Discussion |
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TopAbstractIntroductionMaterials and MethodsResults: Comparability of...DiscussionReferences |
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After serial surgical sacrifice of SAs during aneurysm resection, the perfusion of the spinal cord depends on the stabilization of the collateral network of remaining SAs, fed from below by the hypogastric arteries and from above by the internal thoracic artery and other branches from the subclavian arteries. The pressure conducted through these vessels to the spinal cord, the spinal cord perfusion pressure, is a balance between the inflow and outflow pressures within the closed confines of the spinal canal. The inflow obviously depends principally on arterial pressure, which is largely determined by cardiac output, blood volume, and the competing demands of viscera and muscle tissue connected to the same collateral network. It is therefore not surprising to find that there is an effect of arterial pressure on the development of spinal cord injury. Every aneurysm surgeon has anecdotal cases in which patients have experienced delayed-onset paraplegia after dramatic instances of severe hypotension, even several weeks postoperatively. What is surprising in this study is that the hypotension that precipitated spinal cord injury within the first 48 hours after surgical intervention is quite subtle and depends on viewing appropriate postoperative blood pressure in terms of antecedent ambulatory pressures rather than absolute values. Our neurosurgical colleagues observe loss of intraoperative SSEPs quite often in patients with chronic hypertension if intraoperative blood pressures are not maintained at high normal levels, and MEP or SSEP loss intraoperatively in aneurysm operations, as well as spinal surgery, is often correctible by raising the blood pressure. The findings of this study thus support a policy of maintaining blood pressures at high levels not only intraoperatively, which has even become the practice with endovascular repair, but also for at least 48 hours postoperatively.20,21 This should especially be emphasized in patients with antecedent hypertension.
The finding that a high CVP is also associated with spinal cord injury is somewhat more of a surprise but is quite consistent with the idea that spinal cord perfusion after aneurysm surgery is very precarious. Outflow from the spinal canal depends directly on CSF and venous pressures22 and whether spinal cord edema is present. Tobinick and Vega23 describe the human vertebral venous system as a unique, large-capacity, valveless venous network in which flow is bidirectional and includes the vertebral venous plexuses, which course along the entire length of the spinal cord and anastomose with the intracranial veins in the suboccipital region. Caudally, the vertebral venous system communicates freely with the sacral and pelvic veins and with the prostatic venous plexus. The cerebrospinal venous system plays an important role in the regulation of intracranial pressure and venous outflow from the brain,23 and cerebral venous outflow pathways have been shown to depend on CVP.24 An increased CVP is therefore likely to be reflected by increased pressure in the extensive vertebral venous plexuses25 and would thereby impair spinal cord outflow.
From direct measurements from collateral vessels feeding the spinal cord in pigs and in human subjects, we know that spinal cord perfusion pressures are well below aortic pressures, even at baseline, and that after SA sacrifice, these pressures decrease to a level as low as 20 mm Hg several hours postoperatively.4 At such low values of inflow pressure, it is easy to imagine that a high venous pressure could significantly impede spinal cord perfusion. An appreciation of the vascular anatomy within the spinal canal in pigs shows that branches of the SAs directly supplying the anterior spinal artery have to cross the extensive venous plexuses surrounding the spinal cord, which is likely to be distended with an increased CVP, and therefore a high CVP could also mechanically impede arterial inflow in addition to its effect on outflow.
At these low perfusion pressures, it is easy to imagine that CSF drainage is also important, although the numbers in this study, in which not all patients had spinal cord drainage, are too small to confirm its effect. The effectiveness of spinal cord drainage in reducing the incidence of paraplegia and paraparesis, however, has been firmly established by other investigators.5,26 In 1991, Grum and Svensson22 described a strong positive correlation between intraoperative CSF pressure and CVP (r = 0.9) before aortic crossclamping. In a recent series of 29 patients, Eide and colleagues27 confirmed this finding during and after TAA/A repair (r = 0.8) and observed that the occurrence of neurologic deficits was related to the intraoperative level of CSF pressure, which was greater than 10 mm Hg in the majority of injured patients.
The high early postoperative and 1-year mortality among patients with paraplegia (but not among control subjects) is also not surprising and has been noted in other studies.28,29 We acknowledge that the number of patients in this study is quite small and that the matching for preoperative and intraoperative characteristics is far from perfect. Some factors more common among the control subjects, such as more advanced age and diabetes, would seem to predict a worse prognosis, but others that are more prevalent in the paraplegia group might have contributed to their risk of an adverse outcome, among them chronic obstructive pulmonary disease, emergency operation, and intraoperative clot. Nevertheless, this review of our experience suggests that some cases of paraplegia, with its attendant serious morbidity and high mortality, might be preventable with more meticulous attention to postoperative hemodynamics and fluid management, which is sometimes complicated by concurrent renal failure. The need for a high postoperative blood pressure but a low CVP suggests that use of inotropes is likely to be important in optimizing early postoperative hemodynamics.
Our observations also add weight to the notion that endovascular therapy of these extensive aneurysms might be an achievable goal if accompanied by careful monitoring of spinal cord function and sophisticated hemodynamic management in the immediate postoperative interval, including use of CSF drainage. Direct monitoring of spinal cord perfusion pressure would enable postoperative management specifically addressing the needs of the spinal cord after serial SA sacrifice during open repair or occlusion during endovascular repair.
We recognize that this retrospective study has limitations related to the very small numbers of patients with paraplegia and the difficulty of finding perfectly matched control subjects. Our control subjects were picked blindly and in an effort to allow for changes in technique and experience over time, and all statistical comparisons were carried out in matched pairs. Nonetheless, we cannot be absolutely certain that some unrecognized bias in control patient selection did not occur. Consequently, our findings must be considered suggestive rather than conclusive. But in light of the grave consequences of paraplegia, we believe that even imperfect observations regarding the importance of hemodynamic management during the first 48 hours after TAA/A surgery are worth documenting in the hope that they will add to our understanding of this tragic and possibly avoidable complication.
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Footnotes |
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