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Ann Thorac Surg 1995;59:245-252
© 1995 The Society of Thoracic Surgeons
Department of Surgery, University of Virginia Health Sciences Center, Charlottesville, Virginia
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Abstract |
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 TopFootnotes Abstract IntroductionFrequency of Spinal Cord...Mechanisms of Spinal Cord...Mechanisms of Spinal Cord...SummaryReferences |
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Introduction |
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TopFootnotesAbstractIntroductionFrequency of Spinal Cord...Mechanisms of Spinal Cord...Mechanisms of Spinal Cord...SummaryReferences |
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Frequency of Spinal Cord Injury |
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TopFootnotesAbstractIntroductionFrequency of Spinal Cord...Mechanisms of Spinal Cord...Mechanisms of Spinal Cord...SummaryReferences |
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In the largest series reported on to date, Svensson and associates [1] noted a 16% incidence of paraplegia or paraparesis in 1,509 patients who had undergone repairs for the treatment of thoracoabdominal aortic disease. The complexity of the repair was found to be a significant predictor of spinal cord injury. The Crawford classification defines thoracoabdominal aortic aneurysms as follows: type I, proximal descending thoracic aorta to the upper abdominal aorta; type II, proximal descending thoracic aorta to below the renal arteries; type III, distal half of the descending thoracic aorta into the abdomen; and type IV, most or all of the abdominal aorta.
Repairs of type I, II, III, and IV aneurysms were associated with paraplegia or paraparesis rates of 15%, 31%, 7%, and 4%, respectively. Other authors have also reported an increased frequency of spinal cord injury in patients undergoing repairs of complex (ie, types I and II) thoracoabdominal aortic disease [2, 3].
Repairs limited to the descending thoracic aorta are generally associated with a lower incidence of paraplegia. Livesay and colleagues [3] found the incidence of paraplegia associated with 360 repairs of proximal and extensive descending thoracic lesions was 3% and 9%, respectively. Lerberg and associates [4] reported a 1.5% risk of paraplegia for patients undergoing repair of coarctation of the aorta. Survivors of acute traumatic disruption of the thoracic aorta represent a small subset of patients with thoracic aortic disease. Only 1,188 cases have been reported in the past 20 years; not surprisingly, the incidence of postoperative spinal cord injury varies from 0 to 20% [5–7].
Most authors agree that the presence of dissection or the need for an emergent operation because of aneurysmal rupture increases the risk for spinal cord injury. In Svensson and associates' [1] experience, when dissection occurred, the risk of paraplegia was significantly increased after repairs for all types of thoracoabdominal aortic aneurysms. Livesay and colleagues [3] demonstrated that emergent repairs carried a 17% risk of injury versus a 6% risk for elective repairs. Hollier and co-workers [8] reported a combined paraplegia and paralysis rate of only 5% for 83 elective repairs of nondissecting thoracoabdominal aortic aneurysms.
A frequently debated question with regard to aortic procedures concerns the influence of aortic cross-clamp times on spinal cord injury. Svensson and colleagues [1] determined that the aortic cross-clamp time was an independent predictor of paraplegia or paraparesis. Repairs requiring more than 60 minutes of aortic occlusion carried a 20% risk, whereas the risk for those repairs completed in less than 30 minutes was less than 10%. The median cross-clamp time for all patients in their series was 43 minutes. Likewise, Livesay and co-workers [3] showed that the risk of injury increased from 3% to 11% when the cross-clamp times exceeded 30 minutes.
Conversely, other studies have not shown a clear-cut relationship between spinal cord injury and longer cross-clamp times. In Hollier and associates' [8] series, the cross-clamp times in all 5 patients who suffered postoperative paraplegia or paraparesis were less than 20 minutes. Najafi [9] observed no postoperative spinal cord injury in 31 patients who underwent repairs with mean aortic cross-clamp times of 58 minutes. However, distal aortic perfusion with partial femoral-femoral cardiopulmonary bypass was used in all patients. In a similar report, Svensson and associates [10] concluded that cross-clamp times greater than 40 minutes were not associated with spinal cord injury if distal aortic perfusion was used. Hence, the use of distal aortic perfusion may offset any influence cross-clamp times have on spinal cord injury.
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Mechanisms of Spinal Cord Injury |
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TopFootnotesAbstractIntroductionFrequency of Spinal Cord...Mechanisms of Spinal Cord...Mechanisms of Spinal Cord...SummaryReferences |
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).
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). The superior cord (C1 to T2/T3) is well supplied with three to five anterior radicular arteries. The midthoracic cord (T4 to T7/T8) has only one or no anterior radicular artery. The remaining lower thoracic and lumbar spinal cord is supplied with three to five anterior radicular arteries, including the most important one, the arteria radicularis magna (ARM), or artery of Adamkiewicz [11]. This artery arises between T8 and L3 in 90% of human beings [12] and has a left-sided origin in 80% [13]. Wadouh and associates [14] illustrated the important contribution this artery makes to the lumbar spinal cord blood supply by their finding of a 70% paraplegia rate in pigs after ligation of the artery of Adamkiewicz.
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Spinal Cord Ischemia
Spinal cord ischemia in the perioperative period can result from preoperative hypotension, distal aortic hypotension after aortic occlusion, the interruption of critical intercostal and lumbar arteries, thrombosis and embolism of intercostal arteries, and postoperative hypotension or hypoxia. Neural tissue is exquisitely sensitive to ischemia. At normal temperatures, the stores of adenosine triphosphate are completely depleted after 3 to 4 minutes of ischemia as mitochondrial oxidative phosphorylation ceases. When the adenosine triphosphate levels approach zero, adenosine triphosphate-dependent membrane pumps necessary for intracellular ionic homeostasis fail [19].
This disruption of calcium homeostasis is critically important in initiating the process of irreversible cellular injury. During ischemia, intracellular calcium rapidly accumulates. The increased calcium levels activate the release of cytoplasmic proteases and nucleases, resulting in damage to structural proteins and DNA. Calcium-activated phospholipases metabolize membrane lipids to arachidonic acid and several other vasoactive metabolites. Endothelial xanthine dehydrogenase is converted to xanthine oxidase, an enzyme critical in mediating free radical production during reperfusion [19]. And, finally, an elevated intracellular calcium concentration results in an increased release of the excitatory amino acids aspartate and glutamate, both of which have been shown to be neurotoxic [20].
Reperfusion Injury
Braughler and Hale [21] recently reviewed the current state of knowledge about free radical injury and its importance in ischemic neural tissue after reperfusion with oxygenated blood. Most free radicals are derived from the conversion of molecular oxygen to the superoxide radical by xanthine oxidase in the presence of NADPH (the reduced form of nicotinamide-adenine dinucleotide phosphate) and xanthine or hypoxanthine. Xanthine and hypoxanthine levels rise during ischemia as adenosine triphosphate is quickly metabolized. Other mechanisms of free radical production include the respiratory burst of activated neutrophils that occurs in response to tissue injury, the metabolism of arachidonic acid to prostaglandins G2 and H2, and the autooxidation of catecholamines in the presence of metals such as iron [19]. Free radicals damage DNA, initiate lipid peroxidation, and degrade structural elements like collagen and hyaluronic acid. Lipid peroxidation results in a loss of membrane integrity, inactivation of critical membrane-bound enzyme systems, and an increased ratio of vasoconstrictive prostaglandins like thromboxane A2 [19]. This adverse shift in prostaglandin production can lead to the no-flow phenomenon of microvascular vasospasm and thrombosis secondary to an increased aggregation of platelets and inflammatory cells.
Barone and co-workers [22] observed a significant increase in lower thoracic spinal cord blood flow in dogs compared to the baseline flow after 30 minutes of thoracic aortic occlusion. A significantly greater degree of hyperemia was noted in those dogs with neurologic deficits compared with that seen in neurologically intact dogs. Jacobs and co-workers [23] were able to correlate spinal cord injury with hyperemia and an increased spinal cord blood-brain barrier permeability to albumin, and stated that this increased permeability contributed to the development of spinal cord edema and a possible compartment syndrome. Other authors have correlated a reduction in spinal cord injury with a reduced hyperemic response during reperfusion [24].
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Mechanisms of Spinal Cord Protection |
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TopFootnotesAbstractIntroductionFrequency of Spinal Cord...Mechanisms of Spinal Cord...Mechanisms of Spinal Cord...SummaryReferences |
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The heparin-impregnated Gott shunt can be placed proximally in the ascending aorta, aortic arch, or left ventricular apex, and distally in the descending aorta or femoral artery. Although systemic anticoagulation is not required, a distinct disadvantage of the Gott shunt compared with oxygenated bypass circuits is the lack of control over flow rates and proximal and distal aortic pressures. In two recently published reports concerning series of patients with traumatic tears of the thoracic aorta repaired using the Gott shunt, the incidence of spinal cord injury was not decreased compared with the incidence in those who had cross-clamping alone [5, 7]. However, Verdant and associates [25] reported excellent results with the Gott shunt in patients undergoing elective repairs of thoracic aortic aneurysms.
Femoral vein-to-femoral artery bypass grafting involving the use of a pump oxygenator has the disadvantage of requiring systemic heparinization. The Bio-Medicus pump (Eden Prairie, MN), a heparinless left atrial-to-femoral artery bypass circuit, has been shown to adequately control proximal and distal aortic hemodynamics [26]. This approach appears to be the emerging technique of choice for distal aortic perfusion, especially in patients with traumatic injuries [5, 6]. However, in the setting of nontraumatic thoracoabdominal aortic disease, Crawford and associates [1, 27] and earlier Najafi and colleagues [28] found in their reviews that the rate of paraplegia was either equal to or increased in association with distal aortic perfusion techniques, compared with the rate noted for clamp and repair techniques. Nevertheless, Najafi [9] has more recently reported a zero paraplegia rate associated with distal aortic perfusion using femoral-femoral bypass.
To explain the apparent lack of protection afforded by distal aortic perfusion techniques, Laschinger [29] pointed out that many surgeons fail to properly monitor the spinal cord perfusion pressure and spinal cord function intraoperatively. He stressed the importance of maintaining mean distal aortic pressures greater than 60 mm Hg and of monitoring spinal cord integrity by observing the somatosensory evoked potentials. Somatosensory evoked potentials reflect activity in the sensory tracts of the posterior and lateral spinal cord. Loss of the signal indicates spinal cord ischemia, and this method has been used to assess both the need for and adequacy of distal aortic perfusion.
Intraoperative somatosensory evoked potential monitoring has been criticized for being associated with a significant rate of false-positive and false-negative readings and for its inability to monitor function in the more vulnerable motor tracts of the spinal cord. The monitoring of motor evoked potentials has been shown to be superior to the monitoring of somatosensory evoked potentials because of its high degree of sensitivity and specificity in detecting clinically important motor tract injury. Regardless, Svensson and Crawford [30] have argued that evoked potential recording is of little use, except to confirm the patency of reattached intercostal arteries, if protective measures have been maximally implemented.
Distal aortic perfusion techniques also fail to prevent spinal cord injury when the ARM, the artery critical for furnishing the blood supply to the lower spinal cord, is not perfused. In patients with extensive thoracoabdominal atherosclerotic disease, the ARM is likely to be included in that portion of the aorta being repaired, and therefore it is not perfused by any shunt in the distal aorta. Even with perfusion of the ARM, blood flow to all regions of the spinal cord may not be adequate. Svensson and associates [12] demonstrated in baboons that blood flow to the lower thoracic spinal cord was not increased by a shunt perfusing the ARM even though blood flow to the lumbar spinal cord was increased. This discrepancy was attributed to the smaller diameter and higher resistance in that portion of the anterior spinal artery above the ARM that supplies the lower thoracic spinal cord. They suggested that a similar phenomenon of inadequate perfusion of the lower thoracic spinal cord despite the presence of a functioning shunt exists in human subjects.
INTRATHECAL VASODILATORS.
Several investigators have used the intrathecal route for the delivery of potentially neuroprotective agents. Svensson and colleagues [31] used intrathecally administered papaverine to dilate the anterior spinal artery and found this produced increased lower thoracic spinal cord blood flow and conferred complete protection from paraplegia in a baboon model after 60 minutes of aortic occlusion. In a nonrandomized human trial, a decreased incidence of spinal cord injury was found in those patients receiving papaverine intrathecally via a lumbar catheter [32]. In a dog model of 70 minutes of aortic occlusion, Maughan and co-workers [33] demonstrated uniform protection from spinal cord injury using intrathecal Fluosol, an oxygenated perfluorocarbon possessing known vasodilatory effects.
REATTACHMENT OF INTERCOSTAL AND LUMBAR VESSELS.
In 1986, Crawford and associates published a review [34] of the data in 605 patients who had undergone repair of thoracoabdominal aneurysms and reported an increased risk of neurologic injury in the patients who underwent reattachment of intercostal and lumbar arteries. They attributed this to the increased operative time associated with localizing the vessels that supplied the spinal cord. Preoperative localization using highly selective angiography is also difficult and not without complications [35]. Accordingly, most surgeons forego any attempt to reattach segmental arteries.
Nevertheless, Svensson and co-workers [36] described an intraoperative technique for identifying those arteries supplying the spinal cord that consisted of placement of a platinum electrode on the spinal cord to detect hydrogen ions injected into the segmental arteries. Preservation or division of the arteries so identified significantly influenced the development of postoperative neurologic deficits in pigs. Consequently, they strongly recommend the reattachment of intraoperatively identified intercostal and lumbar arteries be performed in conjunction with distal aortic perfusion or the intrathecal administration of papaverine, or both measures. Similarly, Hollier and associates [8] reported on 24 consecutive patients who underwent thoracoabdominal aortic aneurysm repair with spinal fluid drainage and intercostal reimplantation without a single incident of postoperative paraplegia.
DECREASING CEREBROSPINAL FLUID PRESSURE.
As mentioned earlier, Blaisdell and Cooley [16] believed that the sudden increase in cerebrospinal fluid pressure after aortic occlusion resulted in reduced spinal cord blood flow. They recommended the use of intraoperative cerebrospinal fluid drainage to prevent spinal cord injury. However, animal studies have yielded conflicting results regarding the impact of spinal fluid drainage on spinal cord injury after aortic occlusion [14, 31, 37].
The results of clinical trials have been equally conflicting. McCullough and colleagues [38] kept cerebrospinal fluid pressure to less than 10 mm Hg in 24 patients with nondissecting thoracoabdominal aneurysms and encountered no postoperative neurologic deficits in these patients. Reattachment of the intercostal arteries was performed in some of the patients with extensive disease. Acher and associates [39] reported a 2% incidence of neurologic deficits in 56 patients with thoracic and thoracoabdominal aneurysms whose treatment included spinal fluid drainage and intravenously administered naloxone; this compared with a 23% incidence in control patients. No intercostal reimplantation was performed. Neither of these studies was randomized. In a prospective, randomized trial, Crawford and co-workers [40] found no benefit to using spinal fluid drainage in patients with extensive thoracoabdominal aneurysms regardless of the cerebrospinal fluid pressure during aortic occlusion.
Increasing Spinal Cord Tolerance to Ischemia
HYPOTHERMIA.
Hypothermia causes a generalized reduction in all energy-consuming processes of neural tissue in direct proportion to the degree of cooling [41]. Kouchoukos and colleagues [42] found systemic hypothermic circulatory arrest to be neuroprotective and relatively safe in selected patients with extensive thoracoabdominal disease. However, hemorrhagic, pulmonary, and central nervous system complications limit the widespread application of this technique. Animal models of regional spinal cord hypothermia achieved through intrathecal [43] or arterial [44] perfusion have shown hypothermia to be neuroprotective. More recently, the use of regional perfusion cooling of the spinal cord in human subjects has been reported [45].
ANESTHETIC AGENTS.
Barbiturates like thiopental block synaptic transmission and relax vascular smooth muscle, and have been reported to be neuroprotective in animals [41]. Kirshner and co-workers [46], however, found no benefit provided by thiopental alone, but did find a moderate amount of protection conferred by the combination of thiopental, hypothermia, and superoxide dismutase (SOD). Cocaine-derived local anesthetic agents stabilize cell membranes by inhibiting membrane-bound ion pumps and channels and have been shown to be neuroprotective in animals [47]. Similarly, opiate receptor antagonists like naloxone have been found to cause a decrease in central nervous system metabolic rates and to provide some neuroprotection in animal models of spinal cord ischemia [41, 48].
CALCIUM-CHANNEL BLOCKERS.
Calcium-channel blockers augment cerebral blood flow and neurologic recovery after cerebral ischemia [49]. Schittek and associates [50] observed almost complete protection from spinal cord injury afforded by the intravenous administration of nimodipine after 30 minutes of spinal cord ischemia in pigs. In a rabbit model of spinal cord ischemia, however, Lyden and colleagues [51] found no protective effects conferred by three calcium-channel blockers selective for the cerebrovascular system. They proposed that calcium enters the injured neuron by way of channels other than those blocked by these drugs.
EXCITATORY AMINO ACID ANTAGONISTS.
As mentioned earlier, recent attention has been focused on the excitotoxic neurotransmitter theory of spinal cord injury. Three distinct receptors for aspartate and glutamate have been identified, designated K, Q, and NMDA [20]. Administration of the NMDA receptor antagonists MK801 [48] and LY233053 [52] has been found to provide some degree of spinal cord protection in rabbit models of spinal cord ischemia.
Decreasing Reperfusion Injury
FREE RADICAL SCAVENGERS.
A large body of research has been focused on limiting free radical-induced injury during the reperfusion of ischemic tissue. The intravenous administration of the endogenous free radical scavenger SOD just before and after termination of aortic occlusion in animals was found to protect against ischemic periods of 30 minutes or less [53]. Our laboratory [54] and other authors [46, 53], however, found that SOD alone is not protective against periods of ischemia of 40 minutes or more. With the conjugation of SOD to polyethylene glycol, the half-life of SOD is increased from minutes to hours. Our laboratory [54] and Granke and associates [55] found that this form of SOD alone effects partial but not complete prevention of neurologic injury after 40 and 60 minutes of spinal cord ischemia, respectively.
Despite success in limiting myocardial reperfusion injury [56], the xanthine oxidase inhibitor allopurinol has been shown to be of no benefit in animal models of spinal cord ischemia [31, 53]. Deferoxamine has also been proved beneficial in preventing reperfusion injury in myocardium by chelating free iron, a catalyst for hydroxyl radical formation [57]. Qayumi and colleagues [53] recently reported that deferoxamine is neuroprotective in the setting of spinal cord ischemia; however, a dose-dependent toxicity has been observed [57].
Laschinger and co-workers [58] reported that ischemic spinal cord injury was prevented in animals receiving methylprednisolone intravenously. The protective effects of corticosteroids were thought to be related to their ability to stabilize membranes, modulate the immune system, and scavenge for free radicals. The 21-aminosteroids lack any mineralocorticoid or glucocorticoid activity and are potent scavengers of superoxide and lipid peroxyl radicals, as well as extremely potent inhibitors of iron-dependent lipid peroxidation under in vitro conditions [59]. Fowl and associates [60] reported a decreased rate of spinal cord injury in rabbits given the 21-aminosteroid U74006F intravenously.
IMMUNE SYSTEM MODULATION.
Immune system modulation is a relatively new technique for attenuating reperfusion injury. Giulian and Robertson [61] were able to inhibit the phagocytic and secretory functions of mononuclear phagocytes with chloroquine and colchicine, and demonstrated that the clinical and histopathologic outcomes were improved after 20 minutes of spinal cord ischemia in rabbits treated with these agents. Clark and associates [62] studied the effects of an antibody to the surface glycoprotein CD18, a substance required for leukocytes to adhere to the endothelium, and found a significant reduction in neurologic deficits after 30 minutes of spinal cord ischemia in rabbits given the antibody.
ADENOSINE.
An expanding body of literature has documented the neuroprotective effects of adenosine and its analogues [63–65]. Adenosine-1 receptors are primarily located in the neural tissue, whereas adenosine-2 receptors reside in the smooth muscle and endothelium of the vasculature. The activation of adenosine-1 receptors decreases neuronal and membrane excitability, thereby limiting the damaging influx of calcium through voltage-gated channels. Aspartate and glutamate release is inhibited [63, 64]. Adenosine-2 receptor activation promotes vasodilation, inhibits platelet aggregation, and inhibits neutrophil activation and subsequent free radical production, thus theoretically reversing the tendency toward the no-reflow phenomenon [65]. Recently, in a gerbil model of cerebral ischemia, von Lubitz and Marangos [66] demonstrated significant neuroprotective effects from an exogenously administered adenosine analogue that was given after reperfusion. On the basis of findings from work in our laboratory, we have concluded that a regional infusion of hypothermic adenosine into the excluded infrarenal aorta of the rabbit provides complete protection from spinal cord injury after 40 minutes of spinal cord ischemia, as shown by both clinical and histologic evidence [67].
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Summary |
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TopFootnotesAbstractIntroductionFrequency of Spinal Cord...Mechanisms of Spinal Cord...Mechanisms of Spinal Cord...SummaryReferences |
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Footnotes |
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TopFootnotesAbstractIntroductionFrequency of Spinal Cord...Mechanisms of Spinal Cord...Mechanisms of Spinal Cord...SummaryReferences |
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References |
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TopFootnotesAbstractIntroductionFrequency of Spinal Cord...Mechanisms of Spinal Cord...Mechanisms of Spinal Cord...SummaryReferences |
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