CHAPTER 69 Descending Thoracic and Thoracoabdominal Aortic Surgery
Chapter 68 on aortic arch surgery dealt with definitions and the micropathology of aortic diseases. The discussion of brain protection during deep hypothermia and circulatory arrest is also relevant to descending and thoracoabdominal aortic surgery when deep hypothermia and circulatory arrest are used. The reader is referred to Chapter 68 for a more detailed review. In this chapter, the discussion of central nervous system protection focuses mainly on protection of the spinal cord against injury during descending and thoracoabdominal aortic surgery. The etiologic and predisposing factors, preoperative workup, and operative procedures are also reviewed.
In 2007, we performed 998 aorta operations at our Cleveland Clinic Aorta Center, 258 (86 open and 172 endovascular) on the descending thoracic or thoracoabdominal aorta. Our approach is discussed here.
This chapter discusses the issues associated with nondissecting types of aneurysms of the descending thoracic aorta and thoracoabdominal aorta.1–59 Aortic dissection and dissecting aneurysms are dealt with in Chapters 70, 71, and 72.
Previously, descending thoracic aortic aneurysms were classified according to the extent of involvement and replacement at the time of surgery.45 In a study of 832 descending thoracic aortic aneurysms,45 this classification was used to evaluate the outcome after surgery, namely, the risk for development of a spinal cord neurologic deficit resulting in either paraplegia or paraparesis. After data collection for the analyses, the descending aorta was divided into three equal extents: extent A, the proximal third; extent B, the middle third; and extent C, the distal extent. For the purposes of statistical analyses, these extents were used to determine the incidence of neurologic deficit. The influence of replacing the entire descending aorta was also analyzed. The results of the analyses are discussed under outcomes.
Thoracoabdominal aneurysms were classified by Crawford and others38,44,48 into four extents (Fig. 69-1). Type I thoracoabdominal aneurysms involved the descending aorta proximal to the level of the sixth rib to above the renal arteries; type II thoracoabdominal aneurysms involved the descending aorta proximal to the level of the sixth rib but beyond the renal arteries; type III thoracoabdominal aneurysms involved the distal descending aorta beyond the sixth rib and a variable extent of the abdominal aorta; type IV thoracoabdominal aneurysms involved the abdominal aorta without involvement of the descending aorta. These classifications revealed marked differences between the groups of the expected risk of neurologic deficits involving the spinal cord and, to some extent, the risk of renal failure and mortality. Type II suffered the worst outcomes. Subsequent analyses showed that the risk for development of paralysis in Crawford type I aneurysms varied according to whether the aorta was replaced below the celiac artery.48 Later, it was suggested that type III thoracoabdominal aneurysms should be further divided into a separate group according to the extent of abdominal involvement.26 These aneurysms, however, are seldom seen, and their influence on outcome was not strong enough to warrant a separate classification. Crawford type II thoracoabdominal aneurysms also have varying outcomes according to the involvement of the distal aortic arch and whether the entire abdominal aorta down to the iliacs needs to be replaced.
Figure 69–1 Crawford classification of thoracoabdominal aneurysms. Type I aneurysms extend from the proximal descending aorta to the renal arteries. Type II extends from the proximal descending aorta above the level of T6 to below the renal arteries. Type III extends from below the level of T6 in the descending aorta and into the abdomen to varying extents. Type IV involves predominantly the abdominal aorta.
Congenital lesions of the descending aorta are fairly frequent, in contrast to the thoracoabdominal aorta, in which they are rarely observed.38 The most common congenital lesions involve the distal aortic arch and the proximal third of the descending aorta. In this area, the most frequently occurring lesion is coarctation of the aorta,38 either missed in childhood or seen in patients who have undergone previous surgery for coarctation of the aorta. Not infrequently, multiple operations have been done and patients present as adults with restenosis, an aortic replacement graft or repair that is of inadequate size for an adult, aneurysm formation proximal or distal to the previous repair, or rupture of an old previous repair including, for example, knitted grafts inserted in childhood. A lesion sometimes takes the form of an interrupted aortic arch associated with descending aorta disease. Other congenital lesions include a large Kommerell diverticulum associated with an aberrant right subclavian artery or a right-sided aortic arch (see Chapter 68). Rarely is thoracoabdominal aortic congenital coarctation (sometimes referred to as the middle aortic syndrome) seen. Some of these thoracoabdominal coarctation lesions may be related to other diseases, such as Takayasu’s disease or neurofibromatosis.38 On occasion, aneurysms may be observed in the descending or thoracoabdominal aorta and are most probably the result of chronic congenital infections, particularly from the use of intravenous or arterial cannulas that became infected. We observed this in one of our pediatric patients.38
Medial degenerative aneurysms of the descending or thoracoabdominal aorta are associated with loss of elastic tissues in the aortic wall. Depending on whether cigarette smoking and chronic pulmonary disease are associated factors, there is a variable extent of atherosclerosis within the aortic wall. As aneurysms enlarge, there is an increasing amount of atheromatous material deposition and clot formation within the aneurysms. Areas of clot even appear to resemble aortic dissections on computed tomography (CT) scans or magnetic resonance imaging (MRI). Aneurysms are typically fusiform in nature, although there may be areas of weakness that have a bubble appearance on angiography or magnetic resonance angiography studies. A variant usually seen in older women with long histories of pulmonary disease and cigarette smoking is a penetrating ulcer that can lead to either dissection or, if it is successfully healed, a saccular aneurysm.38 These are most frequently seen in the distal part of the proximal third or middle third of the descending aorta.
Because of extensive atheroma and clot formation in the aneurysms, patients may present with evidence of distal embolization, such as “trash foot,” pancreatitis, abdominal angina, bowel infarction, progressive intermittent claudication, and progressive renal failure. Very rarely, patients are seen with distal embolization from atheromatic and thrombotic lesions in the arch or descending aorta without aneurysms being present. In these patients, a hypercoagulable state is usually found.38
At the time of surgery, if there is extensive clot formation within the aorta in addition to the presence of atheroma, the intercostal vessels will often be obstructed, especially in patients with large aneurysms. In such patients, therefore, collateral sources of blood flow to the spinal cord become critical to maintain spinal cord function.
Furthermore, those patients who have large aneurysms and a long history of medial degenerative aneurysms with extensive atherosclerosis in the aortic wall will show evidence of visceral artery lesions, such as renal artery, celiac artery, and superior mesenteric artery stenoses.42,43 During a period of time, total vessel occlusions will occur.43 Of note, CT scans should be carefully examined for both calcium and atheroma in the distal aortic arch to check if the aortic arch can be safely clamped for more proximal extending medially degenerative aneurysms. The reason for this is the obvious risk of stroke in these patients. If atheroma, clot, or calcium is found, alternative methods for doing the proximal anastomosis should be considered.
Mycotic aneurysms involving only the descending aorta are quite uncommon. More frequently, these occur either in the lesser curve of the aortic arch or, for thoracoabdominal aneurysms, in the area opposite the visceral vessels. Nevertheless, saccular aneurysms of the descending aorta can become infected, resulting in mycotic aneurysms (Fig. 69-2). Similarly, on bacterial culture of clots removed from descending or thoracoabdominal aneurysms, bacteria are often found to be growing within the aneurysms. Of interest, these bacteria appear to have little influence on the postoperative risk of graft or wound infections.
Infection in previously inserted descending or thoracoabdominal grafts can be a complicated problem to manage. The infection may or may not be associated with a left-sided chest empyema, particularly if the patient has recently undergone an operation. Diagnosis can be difficult to obtain. CT-guided aspiration of any fluid around the graft is the most accurate method of determining graft infection. Treatment options include irrigation of the cavity with antibiotics; resection of the infected graft material and placement of a new tube prosthetic graft or an allograft; and resection of the segment of the aorta and oversewing of the aortic stumps with extra-anatomic bypasses, either aorto-abdominal aorta or bilateral axillary-femoral bypasses.32,34,38,44
Traumatic injuries of the aorta are either penetrating or blunt injuries.38 Penetrating injuries require immediate attention because most patients are in shock and have lost large volumes of blood. Most injuries can be repaired by direct suture repair and usually do not require graft insertion. High-velocity missile injuries from either shrapnel or bullets are rarely survived; if the patient does survive long enough to reach the operating room, extensive destruction and secondary injury are usually found.
Blunt injuries of the aorta most commonly occur in the proximal descending aorta at the isthmus.38 Parmley and associates24 performed a study of 275 autopsies and noted that 45% were at the isthmus, 23% in the ascending aorta, 13% in the descending aorta, 8% in the transverse aortic arch, 5% in the abdominal aorta, and 6% in multiple sites. Clinically ascending aortic injuries rarely undergo operation because patients do not survive long enough to reach a hospital. Similarly, only 2% of patients undergo operation for descending aortic tears.38 In approximately one fifth of autopsies in fatal motor vehicle accidents, victims show a ruptured aorta. Multiplane angiography has been the “gold standard” for identification of tears. However, spiral CT with three-dimensional reconstruction or transesophageal echocardiography is being increasingly used for diagnosis.38
Patients with ruptured aortas are often hemodynamically unstable because of either shock or hypertension. Before surgery, while the operating room is being prepared, the patient’s blood pressure needs to be stabilized. The method to use (clamp and sew or distal perfusion with pump, shunt, or cardiopulmonary bypass) to protect the spinal cord during aortic cross-clamping is still debated. In a previous review of 596 patients,40 there were no differences in spinal cord injuries; however, mortality rate was higher with cardiopulmonary bypass. In a more recent review of 1742 patients, Von Oppell and coworkers found that cardiopulmonary bypass and distal perfusion reduced the risk of paralysis.38,58 A prospective multicenter trial reported that clamp and sew (P = .002) and an aortic cross-clamp time exceeding 30 minutes (P = .01) were associated with postoperative paraplegia.12
Available results suggest that both distal perfusion with centrifugal pump and clamp and sew can be equally safe for less than 30 minutes of aortic cross-clamping (Fig. 69-3). With increasing cross-clamp times, usually because of related, more complicated lesions and tears, the risks of paralysis and renal failure increase with both techniques, although less so with distal perfusion.12,38,39,58
Figure 69–3 Relationship between aortic cross-clamp time and the probability of spinal cord injury based on data from traumatic rupture of the aorta and repairs for descending acute dissections. Note: The clamp time for the first 30 minutes is safe; between 30 and 60 minutes, patients are vulnerable; more than 60 minutes, the risk of paralysis is almost certain in this group of patients who have no collateral blood flow and are often in shock. For patients with other types of chronic aneurysms, the curve is shifted farther to the right.
Full cardiopulmonary bypass with circulatory arrest is usually reserved for complicated lesions involving the aortic arch. These lesions are best treated with circulatory arrest after the patient recovers from the initial injury and scar tissue forms so it will hold sutures. In a review of the literature40 of 44 patients initially treated with medical management and subsequently treated with elective surgery, results were excellent. Initial management of patients with traumatic rupture of the aorta associated with complicated injuries of other organ systems or of the aorta is similar to the management of acute aortic dissections of the descending aorta. Patients must be carefully observed in the intensive care unit and treated with antihypertensive medications to ensure that no leakage occurs. It is important to continue to monitor patients carefully for any evidence of leaks for the first week or two.
In patients with traumatic tears of the aorta, the classic site of tears is at the isthmus. These simple tears can often be repaired with a running suture and with the aid of pledgets. In more complicated lesions, a tube graft with a resection of the aorta with end-to-end anastomoses is required (Fig. 69-4). On occasion, aortic dissection is precipitated by trauma, and in this situation, the site of the tear is repaired. The remaining aorta, however, is managed conservatively with careful blood pressure control and follow-up, as with classic types of DeBakey III or Stanford B dissections. Rarely, chronic traumatic saccular aneurysms may resolve spontaneously over time (Fig. 69-5).28 Increasingly, we are now treating traumatic tears with stent grafts. Initial results suggest that mortality risk and risk of paralysis are at least halved.
There is an increased frequency of aortitis associated with giant cell arteritis in the United States and in other countries such as Iceland.38 The reason for this is unknown. In patients with giant cell arteritis of the aorta, it appears that about one third have a history of polymyalgia rheumatica. In addition, approximately 10% of patients with temporal arteritis will typically progress many years later to giant cell arteritis of the aorta.
In patients with giant cell arteritis, the ascending aorta and the aortic arch are enlarged pari passu with the descending aorta or thoracoabdominal aorta. The infrarenal aorta, however, is often spared. Whether this is related to increased collagen content in the infrarenal segment of the aorta or a high elastic content in other segments is not clear.
Tubercular aortitis frequently involves the descending aorta, particularly the mid descending aorta. This is a rare complication of tuberculosis but appears to be related to common antigens found on both the tuberculous bacillus and aortic wall antigens. In contrast, syphilitic aortitis involves the ascending aorta more frequently than the descending or thoracoabdominal aorta.
In the United States, Takayasu’s disease is uncommon, although it is more frequent in patients with a Mediterranean family background. Takayasu’s disease of the aorta has been classified into various categories as illustrated in Chapter 68. Diagnosis is usually based on a symptom complex rather than on aneurysm type. The disease may also transition from an acute phase to a subacute phase before progressing to a chronic phase. Most aneurysms are detected at the chronic stage. Should an aneurysm form at the acute phase, we recommend treatment with steroids, but there is an increased risk of aortic dissection or rupture. In Takayasu’s disease, segments of the aorta may be skipped and spared of inflammatory lesions (see Chapter 68).38 Erythrocyte sedimentation rate and C-reactive protein levels (>1 mg/dL) are useful for following long-term risk of reoperation and activity.
Tumors of the aorta are rare, although when they are found, they tend to occur in the descending and thoracoabdominal aorta segments. In a collected series of these patients from the literature, the prognosis has generally been poor.38 Treatment usually involves resection and graft replacement with or without chemotherapy and radiotherapy.38
Reoperations on the descending and thoracoabdominal aorta are increasing in frequency. For example, in a recent analysis of our patients undergoing surgery, one third had undergone previous descending or thoracoabdominal aneurysm operations, excluding patients who had had previous abdominal aneurysm repairs or ascending arch repairs.50 The reason for this is the natural course of dilatation of the aorta in other unresected segments, particularly if dissected.
The main reasons for reoperation are progression of aneurysmal dilatation of unresected segments of the aorta and either false aneurysm or saccular aneurysm formation after previous repair. In patients who have had previous acute dissection repairs of the ascending aorta, aneurysm formation in the aortic arch and descending or thoracoabdominal aorta is a common entity. Patients who have had previous descending aortic aneurysm replacements will often present with distal degenerative thoracoabdominal aneurysms below the previous descending repair. Less commonly seen are patients who either develop false aneurysms at the various anastomoses or who develop saccular aneurysms of the Carrel patches where intercostal lumbar or visceral vessels have been reattached to a new aortic graft. Albeit rare, this is a problem that should particularly be watched for in patients with Marfan syndrome. Another problem more frequently observed is in that subset of patients with previous stent grafts inserted in the descending aorta who present with complications related to the stent graft (e.g., migration, kinking, or leaks and broken stents) or aneurysm formation distal to the stent grafts. The latter problem is not surprising in that the formation of aneurysms in the aorta tends to be of a progressive nature. Because stent grafts do not limit expansion of the aorta, aneurysm formation at the anastomotic landing sites will often extend beyond the previous stent grafts.38
In questioning patients with descending or thoracoabdominal aneurysms, the most important symptom to elicit and to establish is back pain. The reason for this is that patients with ongoing pain related to the aneurysms are at greater risk of leaking or rupture and operative complications. Back pain, however, can be difficult to distinguish from chronic backaches related to arthritis of the spinal column. Thus, for diagnosis, it is important to search CT scans or MRI scans for any possible evidence of erosion of the vertebral bodies or the ribs by an aneurysm or if the aneurysm is indented by bony structures. Such a finding would indicate that the back pain is related to the aneurysm.
Arch aneurysms associated with descending or thoracoabdominal aneurysms involving the distal aortic arch may be manifested with associated hoarseness or respiratory problems, particularly wheezing related to compression of the left bronchus. The esophagus may also be compressed by the aneurysm at the junction of the aortic arch and the descending aorta or if the descending aorta aneurysm swings into the right side of the chest by being pinched between the vertebral bodies and the aorta. On CT scan, this may appear as a dilated proximal esophagus with fluid and results in dysphagia. Hoarseness is caused by the recurrent nerve’s being stretched by the aneurysm as the nerve wraps around the isthmus of the aorta and the ligamentum arteriosum.38
As mentioned, evidence of distal embolism should be sought in patients with extensive and large aneurysms with contained clot and atheroma. A diagnosis of peripheral vascular disease is often made in these patients, although the reason for peripheral ischemia is related to chronic embolization of atheroma into distal vessels, resulting in arterial occlusion. In patients with medial degenerative aneurysms, presentation of sudden leg weakness and paralysis is uncommon and is more frequently seen with acute dissections. This arises because of interference with spinal cord blood flow, in either the descending or thoracoabdominal segment. In patients with medial degenerative aneurysms and congenital lesions, chronic hypertension is often a factor. Whether chronic hypertension will resolve after the repair of coarctations of the aorta is not certain but is variable. Historical studies have generally shown that approximately two thirds of patients who present as adults with coarctation of the aorta or previous coarctation repairs will continue to have hypertension but usually not as severe as before surgery. Some patients may be normotensive at rest; but during exercise, hypertension is induced as a result of restricted flow to the descending aorta. Thus, a stress test with blood pressure measurement is of value in these patients, both preoperatively and postoperatively. If patients experience exercise-induced hypertension after surgery, even if the surgery is apparently successful, it is often because of an inadequate size graft or a residual narrowed aortic lumen after the repair. For this reason, we recommend that at least a 20-mm tube graft be used in women and, preferably, a 22-mm tube graft or larger in men (see later).
For reasons yet to be determined, smoking plays a much larger role in descending and thoracoabdominal aneurysm formation than in ascending or arch aneurysms. Tobacco addiction with patients currently smoking is a common preoperative problem in patients presenting for descending or thoracoabdominal aneurysm repair. Thus, a history of respiratory problems and a determination of respiratory capacity are essential before descending or thoracoabdominal aneurysm surgery. In a previous prospective study47 examining pulmonary function test results before thoracoabdominal surgery, there was no single cutoff point at which the risk of postoperative respiratory failure, defined as more than 5 days of postoperative ventilation, became significant. Nevertheless, at a forced expiratory volume in 1 second (FEV1) of less than 1.2 L/min, the risks increased considerably. Of course, the patient’s body habitus, including the smaller size of a woman, must be factored into this. Furthermore, if the aneurysm is relatively large, occupying much space in the left side of the chest, respiratory function may improve after resection of the aneurysm, although this is not always the case. Forced expiratory flow FEF25%-75% was found in our prospective study to be the most effective predictor of postoperative respiratory complications. The reason for this is that it gives some indication of the patient’s strength of coughing and thus the ability to clear secretions postoperatively. Also, significant carbon dioxide retention on resting blood gas analysis is a relative contraindication for surgery as is the case for patients receiving chronic supplemental oxygen therapy.38,47
During the history and physical examination, it is clearly important to establish any potential risk factors for and any history of cardiac disease. Thus, patients with atherosclerotic coronary artery disease have significantly greater risk of in-hospital mortality after these types of operations and a poorer long-term survival.38,44 In a previous study, two thirds of the late deaths were related to coronary artery disease.38,44 For this reason and the perioperative risk of myocardial infarction, the presence of coronary artery disease needs to be thoroughly examined. In addition to checking for coronary artery disease, any valvular disease, particularly aortic valve regurgitation, needs to be investigated because during aortic cross-clamping, even with atriofemoral bypass, there is a significant increase in cardiac afterload. If this is associated with aortic valve regurgitation, the patient may go into acute heart failure from myocardial distention. The patient’s left ventricular muscle strength and ejection fractions are also strong determinants of early and late outcome after surgery. Part of the reason for this is that the increased afterload presented to the left ventricle results in a temporary left ventricular dysfunction after surgery, and if the patient has a poor ejection fraction, both the early and late mortality rates are increased. In a study of 132 patients undergoing descending or thoracoabdominal repairs, an interesting finding was that patients who had modest coronary artery disease and did not have coronary bypasses or stents had a higher risk of myocardial infarction and poorer long-term survival than did those who had bypass surgery. This could be in keeping with our current understanding of coronary disease.
A careful search for any renal disease should also be done.42 An increased preoperative creatinine level in the blood has a strong correlation with both operative and late postoperative outcomes. Indeed, it is one of the most important risk factors for both early and late mortality by multivariable analyses.38,42–44 Furthermore, if creatinine levels are significantly elevated, evidence for renal artery stenosis should also be investigated.
Our choice of preoperative testing before descending or thoracoabdominal repair is directed, first, by determination of the extent of resection required and, second, by the prevention of postoperative complications. Most patients will have undergone CT scans, MRI scans, or both of the chest and abdomen, which will document the extent of the aneurysms. In patients with coarctation of the aorta, of particular importance is the need to determine the extent and any gradients. The extent and site of coarctation should be carefully examined by left anterior-oblique views of the aortic arch. Those patients who have had thoracic trauma from either acceleration or, especially, deceleration injuries should have extensive views performed of the distal aortic arch and proximal descending aorta. Of note, accelerating injuries may also cause traumatic rupture of the aorta. We have treated a patient who developed a traumatic rupture of the aorta after being kicked in the chest by a horse. Patients who have extensive aneurysms, especially with a lot of clot and atheroma and renal dysfunction, must have their visceral vessels examined for potential renal artery or celiac or superior mesenteric artery stenoses. This may require a separate magnetic resonance angiography study of the visceral vessels.
All our patients, before elective descending or thoracoabdominal aneurysm surgery, undergo cardiac catheterization and angiography. We ask the cardiologists to do a left anterior-oblique view of the aortic arch at the time of catheterization so that the proximal extent of the aneurysm can be determined because this will influence the operative technique. If coronary artery disease is found at the time of cardiac catheterization, a decision must be made as to the best course of repair management. For example, if it is a single stenosed vessel or a large vessel with a critical area of muscle dependent on it, angioplasty with or without stenting is performed. After this, patients are prescribed clopidogrel (Plavix) for 30 days before elective descending or thoracoabdominal aneurysm surgery is scheduled. Drug-eluting stents are avoided because they require about 3 to 4 months of treatment before open surgery. If extensive three-vessel or left main coronary artery anterior disease is present, the patient should undergo coronary artery bypass surgery before the repair. If the aneurysm involves the proximal descending aorta and the aortic arch, the left subclavian artery may need clamping, and this can interfere with the left internal mammary artery blood supply to the heart. Thus, the options in this situation are either to use a right internal mammary artery bypass graft to bypass the left descending coronary artery or to insert an elephant trunk beyond the left subclavian artery at the time of the use of the left internal mammary artery for the coronary artery bypass surgery. Last, if the patient is found to have more than a 2+ aortic valve regurgitation, the aortic valve needs to be replaced or repaired before surgery. This is due to the potential for acute left ventricular distention leading to heart failure and intraoperative cardiac arrest.
All patients undergo a 24-hour Holter examination because of the high incidence of arrhythmias in this group of patients. This is particularly useful to know because, with arrhythmias, patients who have cooling during the operative procedure may be at greater risk for development of supraventricular arrhythmias, either atrial fibrillation or supraventricular tachycardia.
As indicated before, all patients undergo pulmonary function tests before surgery.47 If the patients are actively smoking and are scheduled to undergo a pulmonary function test, an effort is made to wean the patients off their tobacco dependency and to improve their pulmonary function before surgery. Patients who are actively smoking and undergo thoracoabdominal descending aortic surgery are more prone to prolonged intubation and bronchial secretions after the operation that will complicate their postoperative recovery.
It is essential that all patients have creatinine levels checked before surgery because this measure of kidney function will have a strong influence on early and late outcomes after surgery. Curiously, for reasons that are not entirely clear, the creatinine level after surgery can be surprisingly variable. In most patients, in the first 5 days after surgery, the creatinine level increases. In most of these patients with high creatinine levels after repair of the aneurysm (2 to 3 mg/dL), there is a rapid return to a normal creatinine level as long as the renal arteries have not been treated for stenoses. In a few patients with high preoperative levels, there is a rapid decline to normal levels; this occurs in patients with relatively large aneurysms. An explanation could be that normal pulsatile flow to the renal arteries is interfered with because of the large aneurysms. In patients with significant renal dysfunction (>3 mg/dL) and small kidneys, it is difficult to determine whether renal function will recover after surgery. One possibility is to stent the renal artery stenoses before surgery to see if renal function improves. Although it has not been formally studied, it is our impression that patients with high creatinine levels above 4 to 5 mg/dL before surgery may benefit from preoperative dialysis.
Both the pathophysiology and etiologic factors causing paralysis after descending and thoracoabdominal aneurysm surgery have been extensively reviewed elsewhere.27,36,38,49,50 Briefly, based on both animal and human studies, there are three main mechanisms by which postoperative neurologic deficits and paralysis can arise. First, duration and degree of ischemia during the period of aortic cross-clamping are important. In patients with coarctation of the aorta, there is an extensive collateral network of blood to the spinal cord, so the degree of ischemia is not as severe as in a patient with traumatic rupture of the aorta or acute dissection in which no collaterals have been established to the spinal cord.38,39 In an extensive aneurysm (such as Crawford type II thoracoabdominal aneurysms), the degree of ischemia is more severe because of a greater amount of interference to the spinal cord blood supply. Multiple studies have shown that the duration of ischemia is an important factor. The best way of showing this is by logistic regression analysis of the aortic cross-clamp time or the intercostal ischemia time versus the risk of neurologic deficit (Fig. 69-6; see also Fig. 69-3). The relationship is an S-shaped sigmoid curve, with the risk of paralysis rapidly increasing after 30 minutes of aortic cross-clamping in patients with acute dissection or traumatic rupture of the aorta.38,39 Of interest, in patients with thoracoabdominal aneurysms, because of the extensive collateral blood supply that has been established, the curve is not quite as steep.38,44 Similarly, for descending aortic aneurysms, when there is more direct blood supply below the repair or collateral blood supply, the risk of paralysis after 30 minutes is less. Thus, research shows that the curve is moved to the right by interventions that successfully reduce the risk of spinal cord injury. During the past 2 decades, interventions have successfully reduced the risk of this aspect of spinal cord injury.8,26,27,49,50
Figure 69–6 A, The relationship between aortic cross-clamp time and the risk of paraplegia or paraparesis based on 1508 patients undergoing thoracoabdominal aneurysm repairs according to the Crawford classification of extent (see definitions for extent in the text). B, Influence of aortic cross-clamp time on the risk of paraplegia or paraparesis based on 832 patients with the entire descending aorta replaced. The solid line is for atriofemoral bypass, and the dashed line is for no distal perfusion. Based on logistic regression analysis, after 40 minutes of aortic cross-clamping, atriofemoral bypass did show a protective effect. Atriofemoral bypass was only for the proximal anastomosis at normothermia. C, The relationship between aortic cross-clamp time and the risk of neurologic injury based on a prospective randomized study showing the risk according to no cooling or cerebrospinal fluid drainage or intrathecal papaverine, then the greater protective effect with cerebrospinal fluid drainage and intrathecal papaverine (CSFD + IP), the further greater protective effect of active cooling with atriofemoral bypass, and the greatest protective effect by combining active cooling plus CSFD + IP. Note that this allows a safe aortic cross-clamp time to approximately 60 to 70 minutes. D, Influence of intercostal ischemia time on motor function scores. Note the drop after approximately 50 minutes. Motor score 0, no movement; 1, flicker of movement (e.g., big toe); 2, movement but not against gravity (e.g., sliding a leg while in bed); 3, movement against gravity but weak (e.g., leg raising); 4, normal. E, Influence of intercostal ischemia time on percentage risk of paraplegia or paraparesis based on logistic regression analysis. Note that profound hypothermia and moderate active hypothermia did not have a significantly different risk; however, mild passive hypothermia was associated with a significantly greater risk of paralysis than either moderate active or profound hypothermia (P < .04).
Second, failure to reestablish spinal cord blood flow after clamping of the aorta increases the risk of spinal cord injury. Thus, both animal and human studies have shown that intercostal and lumbar arteries supplying the spinal cord need to be reattached to reduce the risk of postoperative spinal cord and neurologic deficits.27,33,36,38,46,48,52
Third, after the initial ischemic event to the spinal cord, secondary injury can be related to postoperative hemodynamic instability in the intensive care unit after surgery, or the complex biochemical cascade that is set in motion by the initial ischemic injury can result in secondary reperfusion injury, including the development of apoptosis. This complex cascade of multiple pathways of events has been extensively reviewed in detail.35,38,56
Based on the pathophysiology involved in causing neurologic deficits, operative techniques and both experimental and intraoperative maneuvers have been developed to reduce the risks for development of postoperative neurologic incidents.38,44,49,50 Indeed, to address the first etiologic factor (i.e., degree of ischemia and duration of ischemia), certain intraoperative techniques are used. To reduce the risk of ischemia, every attempt is made to shorten both the aortic cross-clamp time and the intercostal ischemia time. Recently, we showed50 the intercostal ischemia time to be a more important variable than total aortic cross-clamp time with respect to neurologic injury. Therefore, quick and efficient anastomoses must be performed during the operation. We recommend the use of techniques that shorten the aortic cross-clamp time, for example, second-stage elephant trunk procedures, whenever indicated. A method we developed in 1992 based on animal experiments is a segmental sequential repair that reestablishes spinal cord blood flow.37,39,49,52 Once proximal anastomosis has been accomplished, the proximal descending aortic and subclavian clamps are removed to reperfuse the subclavian artery and to improve blood flow through vertebral arteries and the posterolateral spinal arteries. The mid descending aorta is cross-clamped during the initial cross-clamping as frequently as possible so that the remaining portion of the aorta below is perfused by the atriofemoral bypass circuit. The intercostal vessels in this segment, down to T6, are oversewn with a 1-0 suture. This segmental level is conveniently in line with the sixth rib, which has been resected during the initial thoracotomy. Next, the aorta is opened down to the clamp placed immediately above the celiac artery, and the intercostal arteries, between T6 and the celiac artery, including any upper lumbar arteries, are then reanastomosed to the graft. If possible, the graft is then de-aired and the intercostal Carrel patches are reperfused, reestablishing further blood flow to the spinal cord through the thoracic radicular arteries so that these collateral vessels can perfuse the anterospinal artery both up and down the length of the spinal artery. After this, the visceral segment of the aorta is repaired, including any lumbar arteries that need to be reattached. This segment is also reperfused both to increase spinal cord blood flow and to reestablish visceral blood flow. In Crawford type II and III thoracoabdominal aneurysms, the lumbar arteries in the abdominal segment are reattached to reperfuse them as well as the median central artery if it is present. Hence, this sequential segmental technique minimizes the period of ischemia to the spinal cord. Both our studies and those by others38,49,50,52 have confirmed that this approach reduces the risk of spinal cord injury. In addition, we have found that cooling of the patients before aortic cross-clamping, either to moderate hypothermia levels, particularly between 30° and 32° C with an atriofemoral bypass circuit,49 or to profound hypothermia levels with cardiopulmonary bypass, reduces the risk of spinal cord injury.50 Both methods appear to be equally effective in protecting the spinal cord.
Other methods of local cooling of the spinal cord include injection of cold solution into the occluded aorta, intrathecal cooling, epidural cooling, and intrapleural cooling alongside the vertebral bodies. Most of these techniques have been shown to be protective in animal studies, but human studies have shown variable degrees of success.2,4,38,46,50
Figure 69–7 A, The aorta gives off intercostal arteries, which in turn give off small anterior or posterior radicular arteries that join the anterospinal or posterolateral arteries. B, The anterior radicular arteries join the anterospinal artery that runs the length of the spinal cord. The arteria radicularis magna (ARM) joins the anterospinal artery as a hairpin bend. The sizes are shown. C, Photograph of ARM and anterospinal artery from postmortem specimen. D, Distribution of ARM origin by vertebral level.