Ann Thorac Surg 2007;84:488-492
© 2007 The Society of Thoracic Surgeons
Original Articles: Cardiovascular
Influence of Perioperative Hemodynamics on Spinal Cord Ischemia in Thoracoabdominal Aortic Repair
Yujiro Kawanishi, MD,
Kenji Okada, MD,
Masamichi Matsumori, MD,
Hiroshi Tanaka, MD,
Teruo Yamashita, MD,
Keitaro Nakagiri, MD,
Yutaka Okita, MD*
Department of Cardiovascular, Thoracic, and Pediatric Surgery, Kobe University Graduate School of Medicine, Kobe City, Hyogo, Japan
Accepted for publication February 28, 2007.
* Address correspondence to Dr Okita, 7-5-2 Kusunoki-Cho, Chuo-Ku, Kobe City, Hyogo, 650-0017, Japan (Email: yokita{at}med.kobe-u.ac.jp).
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Abstract
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Background: The purpose of this study is to investigate the influence of perioperative circulation on spinal cord during the repair of descending thoracic or thoracoabdominal aortic aneurysms.
Methods: From October 1999, 92 patients (aged 66 ± 13 years; 65 men) underwent the repair of descending thoracic (n = 30) or thoracoabdominal aortic aneurysm (Crawford I, 9; II, 14; III, 35; IV, 4). We measured the time duration of hypotension, defined as follows, and evaluated the relationship between the incidence of paraplegia and each duration: T1, systolic arterial pressure less than 80 mm Hg, or mean pressure less than 60 mm Hg during aortic cross-clamping; T2, distal aortic pressure less than 60 mm Hg during aortic cross-clamping; T3, systolic arterial pressure less than 80 mm Hg after coming off bypass; T4, systolic arterial pressure less than 80 mm Hg in the intensive care unit.
Results: Hospital mortality was 8% (7 patients). Neurologic deficits occurred in 10 patients (10.9%). The T1 and T2 periods showed no difference between paraplegia cases (group P) and normal cases (group N). The T3 periods in both groups were 54 ± 52 and 6.6 ± 18, and the T4 periods were 62 ± 89 and 2.3 ± 14, respectively. The T3 and T4 periods in group P were significantly longer than in group N (p < 0.0001). Multivariate analysis demonstrated that T3 was an independent risk factor for paraplegia. When divided according to body temperature, the T2 period under mild hypothermia was significantly longer in group P than in group N, as well as the T3 and T4 periods.
Conclusions: Perioperative hemodynamics stability is of vital importance for spinal cord protection during thoracoabdominal aortic surgery. In particular, the duration of hypotension after coming off bypass was an independent risk factor for paraplegia.
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Introduction
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Paraplegia remains a devastating complication of thoracoabdominal aortic surgery. Hypoperfusion of the spinal cord during aortic cross-clamping (ACC) is one cause of paraplegia after the repair of thoracoabdominal aortic aneurysms. The spinal cord obtains a major blood supply from the segmental radicular arteries, which provide significant flow into the anterior spinal artery [1, 2]. The ischemic insult to the spinal cord during aortic cross-clamping is altered depending on perfusion through the collateral circulation. One important factor that influences collateral circulation is proximal arterial perfusion pressure as well as distal aortic pressure. Postoperative hypotension has been reported as a risk factor of delayed paraplegia after both open surgery and endovascular graft repair of thoracic or thoracoabdominal aortic aneurysm [3–6]. We hypothesized that systemic hypotension during the operation could be a risk factor of paraplegia, although it has not been previously reported, and evaluated the influence of hemodynamics stability on spinal cord ischemia during or after thaoracoabdominal aortic aneurysm repair.
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Material and Methods
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Patients
This study was approved by the Institutional Review Board, and the need for individual consent was waived. Between December 23, 1999, and October 27, 2005, 101 patients underwent the repair of thaoracoabdominal aortic aneurysm or descending thoracic aortic aneurysm. Of these, 92 patients who had neurologic evaluation postoperatively were enrolled in this study. Patients’ ages ranged from 18 to 83 years (mean, 66 ± 13). There were 65 men (71%) and 27 women (29%). Thirty patients had descending thoracic aortic aneurysm. Using the Crawford classification, 9 patients had type I thaoracoabdominal aortic aneurysm, 14 had type II, 35 had type III, and 4 had type IV. Aortic dissection was present in 40 patients (43%) and nondissecting aneurysm in 52 (57%). Six patients (7%) had Marfan’s syndrome and 19 (21%) had ruptured aneurysms. The characteristics of the patients are shown in Table 1.
Surgical Technique
A cerebrospinal fluid drainage catheter was routinely placed into the subarachnoid space on the day before operation. Cerebrospinal fluid was allowed to drain freely whenever cerebrospinal fluid pressure exceeded 10 mm Hg. Transcranial motor evoked potential was applied to monitor spinal cord ischemia during the operation.
The thoracoabdominal aorta was exposed with left thoracotomy, dissection of the retroperitoneal space, and division of the costal cartilage and diaphragm. Cardiopulmonary bypass was established by means of cannulation of the left femoral artery and the right femoral vein, after the administration of heparin (2.0 mL/kg). Mild hypothermia (31°C to 34°C, rectal temperature) was also used routinely to minimize ischemic complications. If cross-clamping of the proximal aorta seemed impossible, deep hypothermia and circulatory arrest were applied.
The aorta was anastomosed to a gelatin-impregnated knitted Dacron graft (C.R. Bard, Haverhill, Pennsylvania) with side branches presewn to reattach segmental and visceral arteries. The aorta was sequentially clamped, and the patent intercostal and lumbar arteries at the Th8 to L2 level were reimplanted and immediately reperfused. Significant back-bleeding from segmental arteries was managed by inserting balloon catheters or by external clamping the segmental arteries to reduce the stealing effect from the anterior spinal artery.
In cases of type II, III, and IV thaoracoabdominal aortic aneurysm, visceral artery perfusion was routinely performed with selective cannulae. Distal anastomosis of the graft and reconstruction of the visceral arteries were completed during rewarming.
Management of Hemodynamics
Proximal and distal arterial pressures were obtained from right radial and right dorsalis pedis arterial catheter, respectively, and mean arterial pressure was managed to between 60 and 100 mm Hg. During cross-clamping, blood pressure was mainly controlled by adjusting the bypass flow of the centrifugal pump. For hypotension, arterial blood pressure augmentation was achieved by the administration of vasopressor agents, volume expansion therapy including blood transfusion, and increased bypass flow.
Collection of Hemodynamic Data
Hemodynamic data for all patients were obtained from anesthesia records, extracorporeal circulation records, and intensive care unit charts, retrospectively. We measured the duration of hypotension, defined as follows (Fig 1): T1 = systolic arterial pressure in the radial artery is below 80 mm Hg, or mean arterial pressure is below 60 mm Hg during aortic cross-clamping; T2 = distal aortic perfusion pressure is below 60 mm Hg during aortic cross-clamping; T3 = systolic arterial pressure is below 80 mm Hg after coming off bypass; T4 = systolic arterial pressure is below 80 mm Hg in the intensive care unit.
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Fig 1. Duration of hypotension. T1 = systolic arterial pressure (SAP) less than 80 mm Hg or mean pressure less than 60 mm Hg during aortic cross-clamping (ACC); T2 = distal aortic perfusion pressure less than 60 mm Hg during aortic cross-clamping; T3 = SAP less than 80 mm Hg after coming off bypass; T4 = SAP less than 80 mm Hg in intensive care unit (ICU). (BP = blood pressure.)
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In anesthesia records, arterial pressure was recorded every 5 minutes and every 10 minutes on extracorporeal circulation records and intensive care unit charts. When arterial pressure was below the criterion pressure at one time, the duration was counted as 5 minutes and 10 minutes, respectively.
Statistical Analysis
Data were processed using Stat View J-5.0 software (SAS Institute, Cary, North Carolina). All values are expressed as the mean ± SE. Statistical analysis was performed with the Mann-Whitney U test to compare the durations between patients with and without postoperative neurologic deficits or between mild and deep hypothermia patients. Unpaired t test was performed only when patients under deep hypothermia were analyzed. Logistic regression multivariate analysis was performed to evaluate the risk factors of spinal cord ischemia. Differences were considered statistically significant at p less than 0.05.
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Results
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Clinical Results
The overall 30-day and in-hospital mortality rates were 3.3% (3 patients) and 7.6% (7 patients), respectively. The causes of death were respiratory failure, gastrointestinal bleeding, and sepsis in 2 patients, and mesenteric ischemia in 1. The overall incidence of paraplegia or paraparesis was 10.9% (10 patients). Of the 10 patients with neurologic deficits, 6 had paraplegia, 3 had paraparesis, and 1 had monoplegia. Five patients (5.4%) were returned to the operating room due to postoperative bleeding. The rates of renal failure, pulmonary complication, and stroke were 7.6% (7 patients), 9.8% (9 patients), and 2.2% (2 patients), respectively. Six patients (6.5%) were successfully treated by catheter interventions because of graft occlusion, with which visceral, renal, and subclavian arteries were reattached.
Evaluation of Hemodynamic Stability
Each period of hypotension in patients with postoperative neurologic deficits (group P) and patients without deficits (group N) is shown in Table 2. The T1 periods in group P and group N were 2 ± 2 and 12 ± 3, and the T2 periods in both groups were 14 ± 9 and 11 ± 4, respectively. The T1 and T2 periods showed no difference between group P and group N. The T3 periods in both groups were 54 ± 17 and 6.6 ± 1.9, and the T4 periods were 62 ± 30 and 2.3 ± 1.5, respectively. The T3 and T4 periods in group P were significantly longer than those in group N (p < 0.0001). Multivariate logistic regression analysis identified T3 periods (odds ratio [OR] 1.058; 95% confidence interval [CI]: 1.005 to 1.114; p = 0.03), prior aortic surgery (OR 3.751; 95% CI: 1.087 to 12.02; p = 0.05), and diabetes mellitus (OR 5.488; 95% CI: 1.452 to 18.89; p = 0.03) as significant independent risk factors for spinal cord ischemia (Table 3).
When divided based on the mode of hypothermia, T1, T2, and T3 periods in patients who underwent operations under deep hypothermia were significantly longer than in patients under mild hypothermia (44 ± 9, 36 ± 14, and 34 ± 10 versus 1.9 ± 1.1, 5.0 ± 1.8, and 5.2 ± 2.1, respectively; p < 0.0001; Table 4). The incidences of neurologic deficits were 11% (8 of 72) in patients under mild hypothermia and 10% (2 of 20) in patients under deep hypothermia (not significant). Among patients under mild hypothermia, T2 was significantly longer in group P than in group N as well as in the T3 and T4 periods (p = 0.03, 0.003, 0.003, respectively; Table 5). On the other hand, T2 was not associated with postoperative paraplegia among patients under deep hypothermia.
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Comment
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The causes of paraplegia after the repair of thoracic or thoracoabdominal aortic aneurysms were believed to be spinal cord ischemia from hypotension during aortic cross-clamping, the interruption of segmental arteries, thrombosis or embolism, and postoperative hypotension or hypoxia.
Midthoracic and thoracolumbar regions of the spinal cord receive their major blood supply from the segmental radicular arteries, which provide significant flow into the anterior spinal artery [1, 2]. During aortic cross-clamping, the spinal cord blood supply depends on spinal cord perfusion through the collateral circulation, such as vertebral arteries, iliolumbar arteries and other segmental arteries. To maximize the collateral circulation, the maintenance of distal aortic perfusion, cerebrospinal fluid drainage, segmental aortic clamping, and reimplantation of intercostal or lumbar arteries have been applied [7–10]. Distal aortic perfusion enables minimization of the ischemic time of distal organs, including the spinal cord, through the lumbar or iliolumbar arteries, and the usefulness of this adjunct has been previously reported [7, 8].
Proximal arterial perfusion pressure is one important factor that influences collateral circulation as well as distal aortic pressure, and some authors reported its importance in an experimental model [11–13]. Lu and colleagues [11] reported the relationship between proximal arterial pressure and spinal cord blood flow during aortic cross-clamping in rats, and concluded that thoracic aortic occlusion with systemic hypovolemic hypotension induced more profound and lasting spinal cord hypoperfusion, which resulted in severe ischemic injury of the spinal cord compared with normal arterial pressure. Taira and coworkers [12] reported a significant proportional correlation between the magnitude of the reduction of proximal arterial pressure and spinal cord blood flow during aortic cross-clamping; moreover, the higher the proximal aortic pressure, the higher the ischemic tolerance. These results implicate the importance of systemic arterial pressure, which affects collateral circulation, to the spinal cord during aortic cross-clamping.
Although it has not been reported that intraoperative hypotension was an independent risk factor in clinical study, Acher and coworkers [14] reported that a significant drop in the cardiac index during cross-clamping was a risk factor for paraplegia. This result may reflect the important contribution of cardiac function to collateralized circulation of the spinal cord.
On the other hand, many authors have recognized postoperative hypotension as a risk factor of delayed paraplegia after both open surgery and endovascular graft repair of thoracic or thoracoabdominal aortic aneurysm [3–6], although preoperative and operative predictors did not include hypotension [15]. Azizzadeh and coworkers [3] reported that mean arterial pressure less than 60 mm Hg and cerebrospinal fluid drain complications increased the incidence of delayed paraplegia after thoracoabdominal aortic open repairs. Chiesa and colleagues [5] reported perioperative hypotension (mean arterial pressure <70 mm Hg) as a significant risk factor of spinal cord ischemia after stent-graft repair of the thoracic aorta. Arterial pressure augmentation and the reduction of cerebrospinal fluid pressure, which restore spinal cord perfusion, have been reported to be effective for delayed paraplegia [4–6, 16].
In our study, systemic hypotension after coming off bypass was revealed to have adverse effects on spinal cord perfusion. The periods of hypotension after coming off bypass and in the intensive care unit (T3 and T4) were longer in patients with postoperative paraplegia than in those with normal spinal function. In particular, T3 was an independent predictor of spinal cord ischemia. This is not because hypotension after coming off bypass deteriorated spinal perfusion most, but because some paraplegia patients suffered serious bleeding or severe hypoxia after coming off bypass, which might have impaired the spinal cord. Actually, in 3 of these patients, motor evoked potentials demonstrated significant ischemic changes in accordance with hemodynamic instability (Fig 2).
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Fig 2. Relation between arterial blood pressure and motor evoked-potential (MEP) monitoring in a patient with postoperative paraplegia. Motor evoked-potential change is shown below the graph. Motor evoked-potential amplitude recovered after transient ischemic change and disappeared in accordance with hemodynamic instability owing to serious bleeding after coming off bypass. The gray bar represents time duration of hypotension. (ACC = aortic cross-clamping; BP = blood pressure.)
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The periods of hypotension during cross-clamping (T1 and T2) were not associated with postoperative paraplegia. This result does not imply that proximal or distal arterial pressure during aortic cross-clamping is not important for spinal cord perfusion. In this study, it is difficult to evaluate the influence of hypotension during aortic cross-clamping because we can maintain sufficient proximal and distal arterial pressure in most patients with ease owing to extracorporeal circulation.
When surgery was performed under deep hypothermia, the duration of hypotension during aortic cross-clamping and after coming off bypass (T1, T2, and T3) was longer than under mild hypothermia, being affected by deep hypothermia and circulatory arrest; however, the incidence of neurologic deficits did not differ in spite of the mode of hypothermia, and the periods of hypotension during aortic cross-clamping (T1 and T2) were not associated with neurologic deficits (Tables 4, 5). This result might reflect the neuroprotective effect of deep hypothermia [17]. The duration of distal arterial hypotension (T2) was longer in group P than in group N only when the operation was performed under mild hypothermia (Table 5). Distal aortic perfusion might be more important, especially in mild hypothermia, under which the protective effect of spinal cord is less than under deep hypothermia, although mild hypothermia is also considered to have this effect [17–19].
In conclusion, perioperative hypotension was associated with spinal cord ischemia and the duration of hypotension after coming off bypass was particularly an independent risk factor for postoperative neurologic deficit. Although proximal and distal arterial pressure during aortic cross-clamping was not revealed to be a significant risk factor for paraplegia, maintaining perioperative hemodynamics was considered of vital importance for spinal cord protection during thoracoabdominal aortic surgery.
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References
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Abstract
Introduction
