(Stroke. 1996;27:2095-2101.)
© 1996 American Heart Association, Inc.
Articles |
Neurological Outcome in a Porcine Model of Descending Thoracic Aortic Surgery
Left Atrial–Femoral Artery Bypass Versus Clamp/Repair
the Departments of Surgery (G.S.M., E.A.P.), Pathology (W.C.H.), and Anaesthesia (H.P.G., W.A.C.M.); the Neuroanesthesia Laboratory (D.B.T., L.G.G.); and the Department of Community Health Science (M.S.C.); University of Manitoba, Winnipeg, Canada.
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Abstract |
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Background and Purpose In a porcine model of thoracic aortic cross-clamping (AoXC), we compared the incidence and severity of paraplegia with two surgical techniques: left atrial–femoral artery (LA-FA) bypass (BP group; n=9) and clamp/repair (CR group; n=8). The descending thoracic aorta was clamped near its origin and distal to the third intercostal artery for 30 minutes. The intervening three intercostal arteries were ligated and divided.
Methods All animals received methohexital anesthesia and were hyperventilated to a PaCO2 of 28 to 32 mm Hg. Animals in the CR group received mannitol, and after AoXC, proximal hypertension was controlled with phlebotomy. In the BP group, proximal hypertension was controlled with LA-FA bypass using a centrifugal pump (Biomedicus 520C). Proximal mean arterial pressure, distal mean arterial pressure, central venous pressure, and cerebrospinal fluid pressure were measured; radioactive microspheres were injected at baseline, at AoXC + 5 minutes, at AoXC + 20 minutes, at AoXC off + 5 minutes, and after resuscitation. Neurological function was assessed at 24 hours. The animals were killed, and the spinal cord was removed to determine spinal cord blood flow. Histological cross sections of the lumbar spinal cord were stained with cresyl violet/acid fuchsin and then examined with light microscopy to determine the ratio of altered to total spinal cord neurons.
Results Fifteen animals survived (one death in each group) and were assessed neurologically at 24 hours after AoXC. Despite better distal perfusion and lumbar spinal cord blood flow in the BP group, during AoXC, and at AoXC off + 5 minutes, there was no significant difference in the severity of spinal cord ischemic injury between groups as assessed neurologically by Tarlov score (P=.90, Mann-Whitney U test). As well, the ratio of altered to total lumbar spinal cord neurons did not differ between groups (P=.24).
Conclusions In this chronic porcine model, distal circulatory support with LA-FA bypass afforded better distal perfusion and improved lumbar spinal cord blood flow but did not influence the severity of spinal cord ischemic injury when compared with a clamp/repair technique.
Key Words: cardiopulmonary bypass • paraplegia • radioisotopes • spinal cord • pigs
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Introduction |
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TopAbstractIntroductionMaterials and MethodsResultsDiscussionReferencesIntroduction |
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Paraplegia occurs as a catastrophic complication of descending thoracic aortic surgery despite an otherwise successful operation. The incidence ranges from a low of 0.5% in coarctation repairs to a high of 40% in acute thoracoabdominal aortic repairs.1 2 3 4 5 Its multifactorial pathophysiology is incompletely understood; however, spinal cord ischemic injury is the final common pathway.6
To facilitate surgical reconstruction, clamping of the descending thoracic aorta (AoXC) is necessary. There are four immediate physiological consequences of AoXC: (1) an increase in MAPp, leading to an increase in cardiac afterload; (2) autotransfusion from the distal (largely splanchnic) vascular beds, which results in a marked increase in the cardiac preload seen as an increased CVP7 ; (3) a marked decrease in the MAPd8 ; and (4) increased CSFP. The marked decrease in ScPP (ScPP equals MAPdminus CSFP or CVP, whichever outflow pressure is greater) coupled with the devascularization incurred by not reattaching critical intercostal arteries contributes to spinal cord ischemic injury and subsequent paraplegia.
Some authors have reported on the hemodynamic and neurological benefits of distal circulatory support during descending thoracic aortic surgery,9 10 11 12 13 whereas others have failed to demonstrate improved neurological outcome.14 15 16 17 These adjuncts can add to the complexity, morbidity, and mortality of thoracic aortic surgery18 19 ; their clinical advantage over a CR approach remains largely unproved. Contributing to this debate are the paucity of randomized prospective studies and the relative abundance of retrospective poorly controlled series.
We designed a randomized prospective experiment to compare the incidence of paraplegia complicating descending thoracic aortic surgery in a chronic porcine model using LA-FA bypass versus a CR approach.
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Materials and Methods |
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Experimental Protocol
This study was approved by the Committee for Animal Experimentation at the University of Manitoba, Canada. The animals were treated according to the guidelines of the Canadian Council on Animal Care. Seventeen female pigs (23±5 kg) were studied. Each animal was premedicated with ketamine (10 mg/kg IM) and atropine (0.6 mg IM), having been fasted overnight. Induction of anesthesia was achieved with isoflurane at 2 minimum alveolar concentrations (2.90%) and maintained at 1 minimum alveolar concentration (1.45%). The trachea was intubated, and the animal was hyperventilated with 100% oxygen to maintain the PaCO2 at 28 to 32 mm Hg. The urinary bladder was catheterized. Catheters were advanced through the left femoral vein into the right atrium to monitor CVP, through the left superficial femoral artery into the distal aorta to monitor MAPd, and into the left internal mammary artery or brachial artery to monitor MAPp. The animal was then placed in a right lateral decubitus position. CSFP was monitored continuously after placement of a spinal needle into the intrathecal space at the L5 level. A 3.0F thermistor was placed into the T5 epidural space through a Tuohy needle to measure epidural temperature. Each animal had a fourth and seventh interspace left thoracotomy. The descending thoracic aorta was encircled 2.5 cm distal to the left subclavian artery origin. The first three dorsal intercostal artery trunks were mobilized, and the aorta again was encircled 1 cm distal to the third intercostal artery trunk. A pigtail catheter, introduced through the aortic arch, was positioned in the left ventricle to allow blood removal and microsphere injection.
All hemodynamics and CSFP were recorded by calibrated Gould P23 transducers referenced at the level of the right atrium. Data were recorded on paper to an oscillograph (Gould 2600S) and onto hard disk using a computer-based (IBM PC-AT) digital acquisition system (Dataq Instruments). Levels of arterial blood gases and hemoglobin were measured before and after each microsphere injection with an ABL-3 Acid-Base Laboratory (Radiometer).
Bipolar leads were placed over the parietal hemispheres, and the electroencephalogram was recorded continuously by an Interspec Medical Neurotrac. A methohexital infusion was administered at 10 mg·kg·-1·h-1 and titrated to an isoelectric electroencephalogram for the duration of the experiment. Nasopharyngeal and thoracic epidural temperatures were monitored and maintained at 37±1°C by use of a heating lamp and pad. All animals were stabilized after surgical intervention for 30 minutes before baseline measurements were taken. Measurements of temperature, MAPp, MAPd, CVP, CSFP, arterial blood gases, and hemoglobin were obtained, and the first microsphere injection was carried out through the left ventricular catheter. Heparin (100 U/kg IV) was circulated (mean activated clotting time, 368±94 s), the proximal and distal thoracic aortas were clamped at the levels of encirclement, and the first three dorsal intercostal artery trunks were doubly clipped (Liga clips) and divided.
Both groups had the AoXC placed for 30 minutes. The CR group (n=8) received mannitol/hyperventilation and had hemodynamic alterations controlled with phlebotomy. Mannitol (2 g/kg IV) was administered to animals in the CR group 30 minutes before AoXC. A previous study indicated that such a dose of mannitol would ensure a diuresis before AoXC.20 After AoXC, these animals were phlebotomized to baseline MAPp and had the blood retransfused just before AoXC release. The BP group (n=9) had distal circulatory support for the duration of AoXC. The LA was cannulated with a 20F DLP atrial cannula and the right femoral artery with a 12F USCI arterial cannula. These were connected to a Biomedicus 520C centrifugal pump. Bypass was initiated just after AoXC, and flow rates were adjusted to achieve baseline MAPp (mean flow, 1.2±0.2 L/min). Mannitol was not administered to animals in the BP group. Preliminary studies indicated that the decrease in preload that follows mannitol diuresis prevents adequate bypass flow rates. Bypass was discontinued just before AoXC release.
Subsequent data sampling and microsphere injections were carried out at AoXC+5 minutes, AoXC+20 minutes, AoXC off+5 minutes, and at 30 minutes after resuscitation back to baseline values. This entailed maintaining a PaCO2 of 28 to 32 mm Hg, supporting an MAPp of less than 50 mm Hg with 20-µg IV adrenaline boluses, 20 to 40 mEq IV sodium bicarbonate if the base excess exceeded 10 mEq/L, and crystalloid administration.
At the end of the experiment, all catheters and cannulas were removed, the thoracotomy was closed, air was aspirated from the pleural space, and wound edges were infiltrated with 0.5% bupivacaine. An intravenous cannula was established in an ear vein, and 0.9% NaCl was administered at 100 cc/h. The animals were also given 0.03 mg/kg IM buprenorphine for analgesia and were extubated. The evening of surgery, they were maintained in a heated pen where they had free access to water. After neurological assessment, they were killed by injection of intravenous Euthanyl. The brain and spinal cord were promptly removed, both kidneys sampled, and materials processed as detailed later.
Neurological Assessment
Neurological injury was assessed by a trained observer not aware of the surgical protocol at 24 hours after the cross-clamp application using a modified Tarlov's paraplegia score21 : grade 0, no voluntary movement or spastic or flaccid paraplegia; grade 1, perceptible movement of joints; grade 2, good movement of the joints but unable to stand; grade 3, ability to stand and walk but absence of attention to knuckling under of limb; and grade 4, intact (no deficit).
Regional Blood Flow Determination
Regional blood flows were determined using radiolabeled microspheres (15 µm) as previously described.22 Approximately 2.5x106 microspheres were injected into the left ventricle, except for the third microsphere injection in the BP group, which was through the right femoral artery. The randomly selected microspheres were labeled with 46Sc, 85Sr, 141Ce, 95Nb, and 113Sn (New England Nuclear). A Harvard syringe pump was used to withdraw blood (20 mL) from the proximal arterial catheter or distal arterial catheter (flow 3, BP group) for 240 seconds, starting 15 seconds before each microsphere injection.
The entire brain was stripped of pia mater and divided into specific regions (left and right frontal, parietal and occipital lobes, basal ganglia, cerebellum, and brain stem). The entire spinal cord was removed, similarly processed, and divided into thoracic (transposed interclamp distance on the thoracic aorta), cervical, and thoracolumbar segments (cephalad and caudad to the thoracic segment, respectively). Tissue and blood samples were placed in a gamma counter (Compugamma 1282) after being weighed. Counts per minute were converted to regional blood flow (milliliters per gram per minute) by computer program using standard equations. Total CBF was determined by summing weighted flows to all brain regions and dividing by the total brain weight.
Histological Analysis
The spinal cord segments were immediately placed in 10% buffered formalin. After fixation, six representative cross-sectional tissue samples were obtained from the lumbar spinal cord and embedded in paraffin. Glass slides containing 7-µm-thick sections were stained with hematoxylin and eosin and cresyl violet/acid fuchsin. An observer, unaware of the animal group and neurological outcome, examined each slide with light microscopy to count the total number of neurons in the anterior spinal cord (anterior to a line drawn through the central canal perpendicular to the vertical axis).23 With cresyl violet/acid fuchsin staining, the neurons were considered significantly altered if hyperchromasia was present, the nucleolus was absent, and the nuclear margin was not distinct.24 With hematoxylin and eosin staining, the cells were considered dead if the cytoplasm was diffusely eosinophilic and viable if the cells demonstrated basophilic stippling (that is, contained Nissl substance). The ratio of altered to total anterior spinal cord neurons was calculated from the cresyl violet/acid fuchsin slides, and the ratio of dead to total anterior spinal cord neurons was calculated from the hematoxylin and eosin slides.
Statistical Analysis
Time-related changes were evaluated with ANOVA for repeated measures. When ANOVA indicated significance for the variable in question, comparisons were made with the least-squares means test. Bonferroni's correction was applied for multiple comparisons, and the corrected probability value was considered significant. Data are presented as mean±SD. Tarlov scores were compared between groups using the Mann-Whitney U test. The ratios of altered to total and dead to total anterior spinal cord neurons were compared between groups using an unpaired t test.
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Results |
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Fifteen animals survived and underwent neurological assessment at 24 hours after AoXC. There was one perioperative death in each group (intraoperative air embolus in the BP group; postoperative respiratory failure in the CR group). These two animals were excluded from neurological and neurohistological assessment.
Temperature, Arterial Blood Gases, and Hemoglobin Data
Table 1
shows data for temperature, arterial blood gases, and hemoglobin levels. Thoracic epidural temperature was minimally greater at baseline and at AoXC+5 minutes in the CR group (0.3°C at both time periods). For the remainder of the experiment periods, temperature did not differ between groups. PaCO2 was stable in the BP group. Similar levels were maintained in the CR group except at AoXC off+5 minutes, when there was a significant increase. Arterial pH was stable in the BP group, while in the CR group an increasing acidosis was seen by AoXC+20 minutes. The acidosis worsened at AoXC off+5 minutes and was only partially corrected at resuscitation. Significant hemoconcentration occurred with mannitol administration in the CR group. The hemoglobin then decreased with phlebotomy but increased again with retransfusion. Hemoglobin level in the BP group remained constant throughout the experiment.
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Hemodynamic Data
After AoXC, in both groups MAPp returned to baseline levels (Table 2). The decrease in MAP at AoXC off+5 minutes was significantly greater in the CR group and corresponded to the greater acidosis experienced by this group. At AoXC+5 minutes and AoXC+20 minutes, MAPd was >75% and <15% of baseline values in the BP and CR groups, respectively. While both groups had decreased MAPd at AoXC off+5 minutes, the decrease was greater in the CR group. CVP and CSFP both remained unchanged from baseline in the BP group. In the CR group, the CVP decreased significantly with phlebotomy, and the CSFP was consistently lower even at baseline than in the BP group due to the effect of mannitol. ScPP values were higher in the BP group during and immediately after AoXC.
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Regional Blood Flow Data
Total CBF was significantly higher in the CR group both during and after AoXC (Table 3). In the post-AoXC period, this corresponded to the increase in PaCO2. The low total CBF and cervical ScBF at AoXC+20 minutes in the BP group were a consequence of the injection of the microspheres into the aorta distal to the AoXC. Otherwise, total CBF and cervical ScBF remained unchanged in the BP group. In both groups, thoracic ScBF was well maintained to AoXC+5 minutes. The low value seen in the third measurement of thoracic ScBF in the BP group demonstrated that there was negligible retrograde perfusion of the thoracic spinal cord segment with LA-FA bypass. Lumbar ScBF was not different between groups at AoXC+5 minutes (when antegrade blood flow to the lumbar cord was measured). Retrograde perfusion of the lumbar spinal cord resulted in significantly higher lumbar ScBF when measured at AoXC+20 minutes in the BP group. In the CR group, lumbar ScBF decreased to 30% of baseline during, and rebounded to 207% of baseline after, AoXC release. In contrast, the lumbar ScBF in the BP group was maintained at approximately 80% of baseline throughout AoXC with no evidence of reactive hyperemia.
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Neurological Outcome
There was no difference in neurological outcome between groups, (P=.90, Mann-Whitney U test) (Table 4). In the CR group, 3 of 7 animals (42.8%) had paraparesis compared with 3 of 8 animals (37.5%) in the BP group.
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Histological Assessment
There was no significant difference between groups in the ratio of altered to total anterior cord neurons in the lumbar spinal cord sections (20.2±6.1 and 24.1±6.4% in BP and CR groups, respectively; P=.24). A representative example of nonviable and viable anterior spinal cord neurons after hematoxylin and eosin staining is shown in the Figure. Only one animal, in the CR group, had evidence of eosinophilic neurons in its lumbar cord with a dead-to-total ratio of 19.3%.
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Discussion |
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We studied neurological outcome in a porcine model of descending thoracic aortic surgery comparing LA-FA bypass with a CR approach. Our failure to demonstrate a difference in neurological outcome between groups is in keeping with the clinical findings of Najafi et al,2 Crawford and Rubio,16 and DeBakey et al,18 all of whom have suggested the prudence of a CR approach. We emphasize that our study is not merely the comparison of a CR technique with a distal support technique, since the CR group may have benefited from what we believe to be optimized anesthetic management. This included mannitol/hyperventilation, phlebotomy, and barbiturate anesthesia, each of which in its own right may ameliorate spinal cord ischemia.20 22 23 We have previously shown mannitol/hyperventilation to be equivalent to CSF drainage without its inherent risks.25 As well, phlebotomy can control the hemodynamic consequences of proximal aortic clamping without compromising ScPP.22
Attempts to prevent paraplegia in descending thoracic aortic surgery must address spinal cord oxygenation and perfusion, both during and after the necessary AoXC. Intraoperative measures include reattachment of critical intercostal arteries and prevention of hypotension.5 In this study, we divided the intercostal arteries between the aortic clamps to simulate a clinical setting where reattachment is not planned or not feasible. As well, perioperative hypotension was treated aggressively.
Although both approaches were effective in treating the increase in MAPp, CVP, and CSFP after AoXC, LA-FA bypass resulted in markedly greater MAPd and hence ScPP during and after AoXC. This would have been expected to have important consequences for spinal cord protection in this group. In addition, improved distal perfusion resulted in a lower PaCO2 and higher pH immediately following AoXC release. The relative hypotension after AoXC release in the CR group had the potential of prolonging the spinal cord ischemic time in this group.26 The lumbar ScBF was much greater in the BP group during AoXC as a direct result of retrograde perfusion of the aorta by the bypass circuit. Reactive hyperemia in the lumbar spinal cord was limited to the CR group after AoXC release. Therefore, given the superior distal perfusion and lumbar ScBF of the BP group, it is surprising that the neurological outcome did not differ between groups. However, others have shown no neurological benefits during clinical use of LA-FA bypass despite improved distal perfusion.15
Importantly, the thoracic ScBF (at the level of devascularized spinal cord) was the same in both groups. The thoracic segment of spinal cord received no benefit from bypass during AoXC in the BP group. Svensson and Hinder14 demonstrated a lack of retrograde perfusion of the thoracic spinal cord in baboons with the thoracic aorta doubly clamped and a thoraco-thoracic shunt in place. They attributed this finding to the discrepancy in size of the anterior spinal artery above and below the point of entry of the artery of Adamkiewicz. In pigs, however, this is most likely due to the discontinuous and plurisegmental nature of the anterior spinal artery, unlike in humans and baboons, where it is continuous but paucisegmental.27 This plurisegmental anterior spinal artery may have rendered the spinal cord less susceptible to catastrophic ischemia after the ligation of only three intercostal arteries. This would appear to be the case, since blood flow in the thoracic spinal cord was not ischemic during, or hyperemic after, cross-clamping.
The CR group had consistently lower CSFP values. Because CSFP was negative during AoXC, CVP became the spinal cord outflow pressure, resulting in mean ScPPs of 11 to 12 mm Hg during AoXC. Oka and Miyamoto, in a canine model, have shown that an ScPP of greater than 7.5 mm Hg is associated with improved neurological outcome.28 Therefore, ScPP in the CR group appears to have been sufficient to prevent more extensive spinal cord ischemic injury. Free radical scavengers have been shown to improve neurological outcome in some studies.5 Mannitol, a known free radical scavenger, may provide spinal cord protection in its own right, as well as favorably altering blood rheology.29 Also, the mannitol-induced diuresis resulted in a significantly higher hemoglobin and arterial oxygen content in the CR group after AoXC release, possibly enhancing oxygen transport to the ischemic spinal cord.20
The absence of greater spinal cord ischemic injury in the CR group, despite the demonstrated lumbar spinal cord hyperemia, suggests that the ischemic lesion at this level was transient. This conclusion is suggested by the similar magnitudes of altered to total anterior spinal cord neurons in both groups from the cresyl violet/acid fuchsin staining technique. Auer et al24 have demonstrated that this dark-cell response represents potentially reversible neuropathology. However, dark neurons with hyperchromasia to all dyes can evolve into acidophilic neurons, which show ultrastructural features of cell death. Only one animal in the CR group had evidence of acidophilic neurons in the lumbar spinal cord at 24 hours, again implying no difference between groups in the severity of lumbar spinal cord ischemia.
Hypothermia, even to a moderate degree, is protective to the spinal cord. In fact, Colon et al30 and Berguer et al31 have shown that local spinal cord hypothermia, using intrathecal iced saline, affords significant spinal cord protection during aortic surgery. There was no difference between groups in thoracic epidural temperatures at AoXC+20 minutes and throughout the resuscitation period, an important controlled variable in our model.
Thus, the key observation from this study is the failure of LA-FA bypass to provide protection to lumbar spinal cord neurons despite essentially normal lumbar ScBF during the period of AoXC. We may not have created a severe enough spinal cord lesion for the neurological benefits of LA-FA bypass to be manifest. However, in preliminary work to establish our model, we experimented with various AoXC durations and felt that an adequate spinal cord lesion was created by 30 minutes. This is supported by the fact that there was hyperemic blood flow in the lumbar spinal cord with AoXC release in the CR group, paraparesis in 3 of 7 animals in the CR group and 3 of 8 in the BP group, and similar histological findings between groups. Although the study size (n=17) may appear too small to achieve adequate statistical power, neurological outcome was very similar, with only a 5.3% difference in paraparesis rate between groups (P=.90, Mann-Whitney U test). To statistically confirm such a 5.3% difference between groups using a one-tailed model (
=0.05; ß=0.2; power, 80%) would require 1237 experiments per group.
Another possible explanation for the lack of benefit may be related to the nonpulsatile retrograde nature of the lumbar ScBF during bypass. Murkin et al32 showed an immediate 37% decrease in the cerebral metabolic rate for oxygen on institution of normothermic, nonpulsatile cardiopulmonary bypass in patients undergoing arrhythmia surgery. Furthermore, Tranmer et al33 demonstrated an increased CBF to both normal and ischemic brain regions in dogs with pulsatile compared with nonpulsatile cardiopulmonary bypass. An experimental comparison of nonpulsatile LA-FA bypass versus pulsatile LA-FA bypass is suggested.
Neurological morbidity can be a consequence of bypass. Microemboli deposition occurs in the brain with cardiopulmonary bypass.34 35 Presumably, microemboli could be deposited in the spinal cord segment that was perfused in a retrograde fashion with partial bypass. As well, MRI techniques have shown cerebral edema to occur in the first hour after coronary artery bypass surgery.36 Thus, failure to demonstrate a neurological advantage with LA-FA bypass may imply that lumbar spinal cord neuronal damage occurs with partial bypass. If so, our findings suggest that the essentially normal blood flow to the lumbar spinal cord during partial bypass may not reflect nutrient blood flow exclusively.
In conclusion, in this porcine model of descending thoracic aortic surgery, LA-FA bypass did not confer any additional spinal cord protection when compared with a technically simpler CR approach using optimized anesthetic management.
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Selected Abbreviations and Acronyms |
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Acknowledgments |
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This research was funded by grants from the Manitoba Northwest Ontario Marfan Association (Dr Pascoe), the Medical Research Council of Canada (Drs Mutch, Pascoe, and Halliday), and the Heart and Stroke Foundation of Canada (Dr Mutch).
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Footnotes |
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Reprint requests to Dr W.A.C. Mutch, Department of Anaesthesia, St Boniface General Hospital, 409 Tache Ave, Winnipeg, Manitoba, Canada R2H 2A6. E-mail mutch@bldghsc.lan1.umanitoba.ca.
Received March 28, 1996; revision received June 26, 1996; accepted July 15, 1996.
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References |
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- Crawford ES, Crawford JL, Safi HJ, Coselli JS, Hess KR, Brooks BB. Thoracoabdominal aortic aneurysms: preoperative and intraoperative factors determining immediate and long-term results of operations in 605 patients. J Vasc Surg. 1986;3:389-404.[Medline] [Order article via Infotrieve]
- Najafi H, Javid H, Hunter J, Serry C, Monson D. Descending aortic aneurysmectomy without adjuncts to avoid ischemia. Ann Thorac Surg. 1980;30:326-335.[Abstract]
- Kouchoukos NT, Rokkas CK. Descending thoracic and thoracoabdominal aortic surgery for aneurysm or dissection: how do we minimize the risk of spinal cord injury? Semin Thorac Cardiovasc Surg. 1993;5:47-54.[Medline] [Order article via Infotrieve]
- Money SR, Hollier LH. The management of thoracoabdominal aneurysms. Adv Surg. 1994;27:285-295.[Medline] [Order article via Infotrieve]
- Shenaq SA, Svensson LG. Paraplegia following aortic surgery. J Cardiothorac Vasc Anesth. 1993;7:81-94.[Medline] [Order article via Infotrieve]
- Marini CP, Cunningham JN. Issues surrounding spinal cord protection. Adv Card Surg. 1993;4:89-107.[Medline] [Order article via Infotrieve]
-
Caldini P, Permutt S, Waddell JA, Riley RL. Effect of epinephrine on pressure, flow, and volume relationships in the systemic circulation of dogs. Circ Res. 1974;34:606-623.
[Abstract/Free Full Text] - Laschinger JC, Izumoto H, Kouchoukos NT. Evolving concepts in prevention of spinal cord injury during operations on the descending thoracic and thoracoabdominal aorta. Ann Thorac Surg. 1987;44:667-674.[Abstract]
- Laschinger JC, Cunningham JN, Nathan IM, Knopp EA, Cooper MM, Spence FC. Experimental and clinical assessment of the adequacy of partial bypass in maintenance of spinal cord blood flow during operations on the thoracic aorta. Ann Thorac Surg. 1983;36:417-426.[Abstract]
- Verdant A, Page A, Cossette R, Dontigny L, Page P, Baillot R. Surgery of the descending thoracic aorta: spinal cord protection with the Gott shunt. Ann Thorac Surg. 1988;46:147-154.[Abstract]
- Coselli JS. Thoracoabdominal aortic aneurysms: experience with 372 patients. J Card Surg. 1994;9:638-647.[Medline] [Order article via Infotrieve]
- Donahoo JS, Brawley RK, Gott VL. The heparin-coated vascular shunt for thoracic aortic and great vessel procedures: a ten-year experience. Ann Thorac Surg. 1977;23:507-513.[Abstract]
- Safi HJ, Bartoli S, Hess KR, Shenaq SS, Viets JR, Butt GR, Sheinbaum R, Doerr H, Maulsby R, Rivera VM. Neurologic deficit in patients at high risk with thoracoabdominal aortic aneurysms: the role of cerebral spinal fluid drainage and distal aortic perfusion. J Vasc Surg. 1994;20:434-443.[Medline] [Order article via Infotrieve]
- Svensson LG, Hinder RA. Hemodynamics of aortic cross-clamping: experimental observations and clinical applications. Surg Annu. 1987;19:41-65.[Medline] [Order article via Infotrieve]
- von Segesser LK, Killer IG, Jenni R, Lutz U, Turina MI. Improved distal circulatory support for repair of descending thoracic aortic aneurysms. Ann Thorac Surg. 1993;56:1373-1380.[Abstract]
- Crawford ES, Rubio PA. Reappraisal of adjuncts to avoid ischemia in the treatment of aneurysms of descending thoracic aorta. J Thorac Cardiovasc Surg. 1973;66:693-704.[Medline] [Order article via Infotrieve]
- Lawrie GM, Earle N, DeBakey ME. Evolution of surgical techniques for aneurysms of the descending thoracic aorta: 29 years experience with 659 patients. J Card Surg. 1994;9:648-661.[Medline] [Order article via Infotrieve]
- DeBakey ME, Cooley DA, Crawford ES, Morris GC. Aneurysms of the thoracic aorta: analysis of 179 patients treated by resection. J Thorac Surg. 1958;36:393-420.
- DeBakey ME, McCollum CH, Graham JM. Surgical treatment of aneurysms of the descending thoracic aorta. J Cardiovasc Surg. 1978;19:571-576.[Medline] [Order article via Infotrieve]
-
Mutch WAC, Graham MR, Halliday WC, Thiessen DB, Girling LG. The use of neuroanesthesia adjuncts (hyperventilation and mannitol administration) improves neurological outcome following thoracic aortic cross-clamping in dogs. Stroke. 1993;24:1204-1211.
[Abstract/Free Full Text] - Tarlov IM. Spinal Cord Compression-Mechanisms of Paralysis and Treatment. Springfield, Ill: Charles C Thomas Publishing; 1957.
- Mutch WAC, Thomson IR, Teskey JM, Thiessen DB, Rosenbloom M. Phlebotomy reverses the hemodynamic consequences of thoracic aortic cross-clamping: relationships between central venous pressure and cerebrospinal fluid pressure. Anesthesiology. 1991;74:320-324.[Medline] [Order article via Infotrieve]
-
Mutch WAC, Graham MR, Halliday WC, Teskey JM, Thomson IR. Paraplegia following thoracic aortic cross-clamping in dogs: no difference in neurological outcome with a barbiturate versus isoflurane. Stroke. 1993;24:1554-1560.
[Abstract/Free Full Text] - Auer RN, Olsson Y, Siesjo BK. Hypoglycemic brain injury in the rat: correlation of density of brain damage with the EEG isoelectric time: a quantitative study. Diabetes. 1984;33:1090-1098.[Abstract]
- Mutch WAC, Thiessen DB, Girling LG, Graham MR. Neuroanesthesia adjunct therapy (mannitol and hyperventilation) is as effective as cerebrospinal fluid drainage for prevention of paraplegia after descending thoracic aortic cross-clamping in the dog. Anesth Analg. 1995;81:800-805.[Abstract]
- Crawford ES, Svensson LG, Hess KR, Shenaq SS, Coselli JS, Safi HJ, Mohindra P, Rivera V. A prospective randomized study of cerebrospinal fluid drainage to prevent paraplegia after high-risk surgery on the thoracoabdominal aorta. J Vasc Surg. 1990;13:36-46.
- Wadouh F, Lindemann E, Arndt CF, Hetzer R, Borst HG. The arteria radicularis magna anterior as a decisive factor influencing spinal cord damage during aortic occlusion. J Thorac Cardiovasc Surg. 1984;88:1-10.[Abstract]
- Oka Y, Miyamoto T. Prevention of spinal cord injury after cross-clamping of the thoracic aorta. J Cardiovasc Surg. 1987;28:398-404.[Medline] [Order article via Infotrieve]
-
Little JR. Modification of acute focal ischemia by treatment with mannitol. Stroke. 1978;9:4-9.
[Abstract/Free Full Text] - Colon R, Frazier OH, Cooley DA, McAllister HA. Hypothermic regional perfusion for protection of the spinal cord during periods of ischemia. Ann Thorac Surg. 1987;43:639-643.[Abstract]
- Berguer R, Porto J, Fedoronko B, Dragovic L. Selective deep hypothermia of the spinal cord prevents paraplegia after aortic cross-clamping in the dog model. J Vasc Surg. 1992;15:62-72.[Medline] [Order article via Infotrieve]
- Murkin JM, Farrar K, Tweed AW, Guiraudon G. The influence of non-pulsatile normothermic perfusion on cerebral blood flow and metabolism. Anesth Analg. 1987;66:S125. Abstract.
- Tranmer BI, Gross CE, Kindt GW, Adey GR. Pulsatile versus nonpulsatile blood flow in the treatment of acute cerebral ischemia. Neurosurgery. 1986;19:724-731.[Medline] [Order article via Infotrieve]
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Moody D, Brown W, Challa V, Stump D, Reboussin D, Legault C. Brain microemboli associated with cardiopulmonary bypass: a histologic and magnetic resonance imaging study. Ann Thorac Surg. 1995;59:1304-1307.
[Abstract/Free Full Text] -
Mills S. Risk factors for cerebral injury and cardiac surgery. Ann Thorac Surg. 1995;59:1296-1299.
[Abstract/Free Full Text] - Harris DNF, Bailey SM, Smith PLC, Taylor KM, Oatridge A, Bydder GM. Brain swelling in first hour after coronary artery bypass surgery. Lancet. 1993;342:586-587.[Medline] [Order article via Infotrieve]
Editorial Comment
Left Atrial–Femoral Artery Bypass Versus Clamp/Repair
Department of Neurological Surgery, Wayne State University, Detroit, Mich
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Obviously, the important message of this study, which compares spinal cord ischemia with and without bypass, is that it makes no difference in this particular model. The authors state that in the bypass group, cerebral blood flow values were artificially low because the microspheres were injected distal to the aortic clamp, but I wonder whether this was not also the case for cervical and thoracic spinal cord blood flow. It is conceivable that under these low-perfusion-pressure circumstances there is retrograde flow from the vertebral arteries all the way down to the thoracic cord. Thus, I would not attach too much significance to the values for cervical and thoracic spinal cord blood flow reported in this article.
The authors have explained well why the group without bypass received a high dose (2 g/kg) of mannitol before cross-clamping, but this explanation does not exclude the possibility that this may have made a difference in neurological outcome. The argument is made that it would take 2474 experiments to confirm the 5.3% difference in outcome in favor of the bypass group. I would rather have seen the confidence intervals of the present difference. Nevertheless, only a randomized clinical trial could resolve the issue, and with the present findings I doubt it would be worth pursuing.
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CR group, n=7; BP group, n=8.
P=.90, Mann-Whitney U test.
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