Tips for Successful Outcomes for Descending Thoracic and Thoracoabdominal Aortic Aneurysm Procedures Joseph S. Coselli, MD, and Scott A. LeMaire, MD The continuing evolution of endovascular approaches to the repair of descending thoracic and thoracoabdominal aortic aneurysms necessitates careful evaluation of the safety and efficacy of these alternative therapies as they compare to the “gold standard” of open surgical repair. The purpose of this report is to present our approach to conventional open surgical repair of these aneurysms. Routine surgical modalities include use of moderate systemic heparinization, mild permissive hypothermia, and sequential aortic clamping. For extensive thoracoabdominal and select descending aortic procedures, additional modalities are used. The multimodal approach to organ protection during surgical treatment of descending thoracic and thoracoabdominal aneurysms has evolved substantially over the past 20 years. Experienced surgical centers now have much lower mortality and morbidity rates for these operations than previously reported. Current management strategies enable patients to undergo conventional open aneurysm repairs with excellent early survival and acceptable morbidity. Semin Vasc Surg 21:13-20 © 2008 Elsevier Inc. All rights reserved.
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URGICAL TECHNIQUES USED during descending thoracic and thoracoabdominal aortic aneurysm (DTA and TAAA, respectively) repair have evolved significantly during the past 20 years. Although open surgical repair of these aneurysms once entailed great operative risk, experienced surgical centers now have much lower mortality and morbidity rates for these repairs than reported previously.1,2 Specific surgical techniques to reduce mortality and prevent end-organ ischemia have emerged, and surgical repair is widely considered the “gold standard.” Nonetheless, managing patients during and after DTA or TAAA operations remains challenging, as postoperative complications may develop because of the inherent complexity of these repairs. Preoperatively, a thorough patient assessment may reveal preexisting cardiovascular, pulmonary, or renal risk factors, thus enabling development of a customized approach to open repair. For example, because tobacco use is a major risk factor for development of TAAAs, it is not uncom-
Division of Cardiothoracic Surgery, Michael E. DeBakey Department of Surgery, Baylor College of Medicine and The Texas Heart Institute at St. Luke’s Episcopal Hospital, Houston, TX. Address reprint requests to Scott A. LeMaire, Division of Cardiothoracic Surgery, Michael E. DeBakey Department of Surgery, Baylor College of Medicine, One Baylor Plaza, BCM 390, Houston, TX 77030. E-mail:
[email protected]
0895-7967/08/$-see front matter © 2008 Elsevier Inc. All rights reserved. doi:10.1053/j.semvascsurg.2007.11.009
mon for TAAA patients to present with compromised pulmonary function. Similarly, patients with Marfan syndrome, even those who are relatively young, often present for surgical intervention in suboptimal pulmonary condition. Diaphragm-sparing techniques may be particularly helpful in patients with poor pulmonary reserve.3 Patients in poor health and with extensive aneurysms remain at increased risk for postoperative complications. Patients who undergo replacement of the entire thoracoabdominal aorta (extent II) continue to have the highest rates of early death, spinal cord deficit, and renal failure.4 As the population ages and diagnostic capabilities improve to better identify DTAs and TAAAs, elderly patients with relatively limited physiologic reserve are increasingly being referred for treatment. Thus, there is a continuing need to develop and refine treatment strategies. Largely because of the morbidity and mortality associated with open DTA and TAAA repair, endovascular approaches have become particularly attractive. However, to justify the use of these approaches, their associated mortality and morbidity rates must be clearly shown to be equal to or better than those of open surgical repair.
Intraoperative Strategies The rationale for and technical aspects of our current method of DTA and TAAA repair have been described in detail (Figs 13
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Figure 1 The clamp-and-sew technique (A, B) for repair of a descending thoracic aortic aneurysm. (A) Exposure is achieved through a posterolateral thoracotomy (inset). Clamps are placed on the aortic arch (between the left common carotid and left subclavian arteries) and on the left subclavian artery. The aorta is opened longitudinally and divided circumferentially a few centimeters beyond the proximal clamp. (B) After the proximal anastomosis is completed, the aortic clamp is repositioned onto the graft, flow is restored to the left subclavian artery, and the remainder of the aneurysm is opened longitudinally. An open distal anastomosis completes the repair. (C) As an alternative to the clamp-and-sew technique, left heart bypass can be used selectively to provide distal aortic perfusion during the repair.
1 and 2).5 Because organ ischemia remains a major source of morbidity related to DTA and TAAA repair, we use a multimodal approach that is based on the extent of disease to maximize organ protection during these open operations (Table 1). Moderate systemic heparinization, mild permissive hypothermia, and sequential aortic clamping are routinely used in DTA and TAAA repairs. These and other important strategies have been used successfully in our practice. Additional protective strategies used elsewhere include motor
evoked potential monitoring, epidural cooling, and routine use of hypothermic circulatory arrest.6-8 A posterior lateral thoracotomy or a thoracoabdominal exposure is used as the surgical approach in all cases.
Moderate Heparinization We consistently administer intravenous heparin (1.0 mg/kg) before aortic clamping. This precaution prevents initiation of
Management of descending and thoracoabdominal aortic aneurysms the clotting cascade, thereby preserving microcirculation, preventing embolization, and aiding in the reduction of disseminated intravascular coagulation. Although the use of heparin during DTA and TAAA repair is controversial, we believe that preventing possible thrombosis of intercostal and lumbar arteries and, thus, avoiding potential spinal cord infarction warrants the use of heparin. Potential complications include coagulopathy and bleeding, although these have rarely occurred in our practice.9 To reverse the effect of heparin, protamine sulfate is given after the final anastomosis is completed.
Mild Permissive Hypothermia Because the benefits of general hypothermia are well-established, we routinely allow the core body temperature to drift down to a target range of 32° to 34°C. After the repair is completed, we irrigate the operative field with warm saline to reverse cooling. Whenever the aorta cannot be safely clamped (as in patients with very large or extensive aneurysms or extremely atherosclerotic or friable aortic tissue), selective use of hypothermic circulatory arrest is warranted. Although the surgical techniques and target temperature ranges for hypothermia differ among treatment centers, the goal—to use cold temperatures to protect the spinal cord and kidneys—is consistent.
Sequential Aortic Clamping The hemodynamic effects of clamping and unclamping the aorta have been investigated since the mid-20th century because these effects are major contributors to the development of postoperative organ dysfunction. Sequential clamping of the aorta remains an effective strategy for reducing ischemic times. In this technique, as the aorta is replaced from the proximal to the distal extent of the lesion, the aortic clamp is moved sequentially to lower positions along the graft to restore perfusion to newly reattached branch vessels.
Cerebrospinal Fluid Drainage Spinal cord ischemia and consequent paraplegia or paraparesis are considered the most devastating complications of surgical DTA and TAAA repair. This type of ischemic complication can result from the complex interactions between perfusion, oxygen supply and demand, local metabolic rate, and reperfusion injury. Early experimental data showing that cerebrospinal fluid (CSF) pressure rises during aortic clamping10 led to development of mitigating strategies to reduce CSF pressure; CSF drainage was shown to reduce CSF pressure and improve spinal cord perfusion.11 The findings of several clinical studies, including our own published results, support the protective role of CSF drainage during TAAA repair.12-16 In our study of 145 patients undergoing extent I or II TAAA repairs and randomized to either CSF drainage or no CSF drainage, we found that only two patients (3%) in the CSF drainage group had postoperative paraplegia or paraparesis, whereas nine patients (13%) in the control group did (P ⫽ .03).13 Rarely, complications such as
15 intracranial bleeding, perispinal hematoma, or meningitis can develop. Thus, we generally reserve this technique for Crawford extent I and II TAAA repairs, whose anticipated benefits outweigh these risks.17-19 For CSF drainage, we insert an 18-gauge intrathecal catheter through the second or third lumbar space immediately after induction. Fluid is passively drained for roughly 48 hours. A target CSF pressure of 10 to 12 mm Hg is maintained throughout the operation and early postoperative period, and the target pressure is increased to 12 to 15 mm Hg once patients have confirmed that they are able to move their legs. Before removing the CSF drainage catheter, we commonly clamp it for several hours to confirm that discontinuing CSF drainage will not precipitate a delayed deficit. We recently studied the characteristics of postoperative spinal cord deficits that we encountered during a 19-year experience with 2,368 TAAA repairs, and we found that 93 patients (3.9%) had postoperative paraplegia or paraparesis. Fifty-nine of these patients (63%) had the deficit immediately upon awakening from anesthesia; 34 patients (37%) had normal neurologic function upon awakening, and a delayed deficit developed subsequently. In 9 (26%) of the patients with delayed paraplegia, onset of the deficit was precipitated by an episode of hypotension.20 CSF drainage is an important component of treatment in patients with both immediate and delayed deficits.
Segmental Artery Reattachment Intuitively, the reattachment of segmental arteries should prevent spinal cord injury by preserving circulation to the anterior spinal artery; however, among clinical practices, the issue of which specific arteries to ligate and which to reattach remains in dispute. Although Griepp and Griepp21 have recently described their “collateral network concept” detailing the redundancies in the blood supply to the spinal cord and questioning the usefulness of segmental artery reattachment, we and others believe that the anatomic complexities of the spinal cord circulation—the commonly incomplete anterior spinal artery, for example, as well as individual anatomic variations among patients (including the varying location of the artery of Adamkiewicz)—warrants aggressive reattachment strategies. Indeed, most authors favor preserving at least some intercostal and lumbar arteries in the critical region of T8-L1. Proximal to T6, we oversew segmental arteries, but in the T7-L2 region, we generally reattach one to three pairs, performing more extensive reattachment in patients with compromised collateral flow (such as patients with a history of prior abdominal aortic surgery and those requiring concomitant iliac aneurysm repair). If severe intimal atherosclerosis obliterates all intercostal and lumbar arteries, an endarterectomy may be required to identify arteries suitable for reattachment.
Left Heart Bypass Temporary disruption of blood flow to the spinal cord and abdominal viscera, if prolonged, has the potential to signifi-
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Figure 2 Repair of an extent II thoracoabdominal aortic aneurysm (A) that extends from the left subclavian artery to the aortoiliac bifurcation. (B) Perfusion systems used during the repair include a left heart bypass circuit (to provide distal aortic perfusion) and a cold renal delivery system (to provide selective renal hypothermia). The proximal portion of the aneurysm is isolated between clamps placed on the aortic arch (between the left common carotid and left subclavian arteries), the mid-descending thoracic aorta, and the left subclavian artery. (C) Whenever possible, the phrenic, vagus (indicated by X), and recurrent laryngeal nerves are preserved during the repair. The isolated segment of aorta is opened longitudinally and divided circumferentially a few centimeters beyond the proximal clamp. (D) Patent intercostal arteries in this region are oversewn. (E) Continuous polypropylene suture is used for the proximal anastomosis. (F) Left heart bypass is stopped, the proximal clamp is repositioned onto the graft, flow is restored to the left subclavian artery, and the remainder of the aneurysm is opened longitudinally. (G) Balloon perfusion catheters are inserted into the celiac and superior mesenteric arteries to deliver selective visceral perfusion from the left heart bypass circuit, and into the renal arteries to intermittently deliver cold crystalloid. Patent lower intercostal arteries are reattached to an opening in the graft. (H) Sequential aortic clamping is used to restore intercostal perfusion. The celiac axis, superior mesenteric, and right renal arteries are reattached to an opening in the side of the graft. (I) Sequential aortic clamping is used to restore visceral and right renal perfusion. The mobilized left renal artery is reattached. (J) Sequential aortic clamping is used to restore left renal perfusion. The distal anastomosis at the aortoiliac bifurcation completes the repair.
cantly contribute to ischemic complications. By maintaining distal aortic perfusion during aortic reconstruction, left heart bypass (LHB) reduces spinal and visceral ischemic time. Patients undergoing the most extensive repairs seem to benefit greatest from LHB. In our own retrospective review of 1,250
consecutive extent I and extent II TAAA repairs, we found that LHB reduced the incidence of spinal cord deficits only in patients with extent II repairs.1,9 For patients undergoing extent I repairs, the significantly longer aortic clamp times in the LHB group did not increase the incidence of paraplegia
Management of descending and thoracoabdominal aortic aneurysms
Figure 2 (continued)
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18 Table 1 Current Strategy for Spinal Cord, Visceral, and Renal Protection During Thoracoabdominal Aortic Aneurysm Repair All extents Moderate heparinization (1 mg/kg) Permissive mild hypothermia (32-34°C, nasopharyngeal) Aggressive reattachment of segmental arteries, especially between T8 and L1 Perfusion of renal arteries with 4°C crystalloid solution when possible Sequential aortic clamping when possible Extents I and II Cerebrospinal fluid drainage Left heart bypass during proximal anastomosis Selective perfusion of celiac axis and superior mesenteric artery during intercostal and visceral/renal anastomoses
relative to that of the no-LHB group. This finding suggests that LHB allows more time to create a secure proximal anastomosis because the spinal cord is protected. In our experience with 666 extent I and II repairs performed with LHB, the incidence of postoperative paraplegia/paraparesis and renal failure was 3.9% and 5.3%, respectively.9 An increasing amount of retrospective data also supports the use of LHB to reduce the risk of ischemic complications.1,9,15,22,23 Additionally, LHB is used in patients with poor cardiac function because it effectively unloads the heart. In patients undergoing Crawford extent I or II repairs, we routinely use LHB during the proximal anastomosis, establishing a temporary bypass from the left atrium to either the femoral artery or the distal descending thoracic aorta with a closed-circuit, in-line centrifugal pump that lacks a cardiotomy reservoir, oxygenator, or warming device.
J.S. Coselli and S.A. LeMaire placed within the origins of the celiac axis and superior mesenteric artery and are connected to the LHB circuit by a Y-line from the arterial perfusion line. Oxygenated blood flows to the abdominal viscera while the intercostal and visceral branches are reattached to the graft. This technique effectively reduces the total mesenteric ischemic time to just a few minutes for even the most complex aortic reconstructions.
Minimizing Ischemic Time It is generally accepted that outcomes in TAAA repair are highly dependent on the duration of intraoperative organ ischemia. It follows that shorter aortic clamp times limit organ ischemia and decrease the risk of renal, visceral, and spinal cord complications. The traditional clamp-and-sew techniques of TAAA repair have been shown to be effective in experienced surgical centers.28 Central to this approach is an expedient and efficient reconstruction performed by a dedicated team. Institutional commitment on the part of hospital administrations to provide sufficient resources, surgeons, anesthesiologists, nurses, perfusionists, pathology support, and blood banking is critical. As mentioned, we advocate the selective use of ischemia-reducing surgical adjuncts as dictated by a patient-specific operative approach.
Monitoring and Postoperative Strategy
Whenever possible, we protect the kidneys by intermittently perfusing them with cold (4°C) crystalloid to maximize renal hypothermia. This practice is supported by results of a clinical trial we conducted in patients who underwent Crawford extent II TAAA repairs with LHB.24 Patients were randomized to receive renal artery perfusion with either cold crystalloid (lactated Ringer’s solution) or normothermic blood from the LHB circuit. We found that cold crystalloid perfusion provided better protection against acute renal dysfunction. Additional studies also suggest that selective renal perfusion during TAAA repair improves outcomes.24-26
Initial postoperative strategy focuses on monitoring for emerging complications while optimizing oxygen delivery, volume status, and cardiac output. A very narrow range of blood pressure is maintained during the first 24 to 48 hours. Because aortic anastomoses are often extremely fragile during the early postoperative period, blood pressure that is too high may disrupt suture lines, causing severe bleeding or pseudoaneurysm formation. However, blood pressure that is too low must also be avoided, as it can precipitate ischemic complications, including paraplegia and renal failure. We try to keep mean arterial blood pressure between 80 and 90 mm Hg by using intravenous -antagonists and nitroprusside. In patients with certain specific profiles (such as patients with Marfan syndrome), a lower target range of 70 to 80 mm Hg is used. Anemia is treated aggressively with transfusion. Patients are allowed to awaken gradually from anesthesia, after which their neurologic function is assessed. The patient is sedated until the next morning, and recovery focuses on reducing ventilator settings, preparing for extubation, and, during the next few days (ideally), preparing for hospital discharge.
Selective Visceral Perfusion
Managing Early Organ Dysfunction
Distal aortic perfusion provides flow to the mesenteric and renal branches only during the initial portion of a TAAA repair. Although clinically significant postoperative manifestations of hepatic, pancreatic, and bowel ischemia are infrequent, they can have devastating impact when they occur. To reduce the risk of perioperative coagulopathy and bacterial translocation,27 after the aorta is opened adjacent to the visceral branches, separate balloon perfusion catheters are used to selectively perfuse the visceral arteries. These catheters are
Respiratory complications are the most common form of morbidity after TAAA repair, in part because of the large volumes of fluids administered intraoperatively and postoperatively; these complications are especially prevalent in patients with preoperative renal insufficiency.2,29 Strategies for managing respiratory complications are varied and specific to each patient’s needs but may include reintubation and a return to ventilator-assisted breathing; a tracheotomy; medical therapy, such as the use of furosemide, inhalers, or antibiot-
Cold Crystalloid Renal Perfusion
Management of descending and thoracoabdominal aortic aneurysms ics; bronchoscopy; use of nebulizers; thoracentesis or placement of a chest tube for drainage of effusions; and surgical treatment of left vocal cord paralysis. For emerging paralysis or paraparesis, treatment involves inserting a CSF drain (if not already present), correcting anemia, and optimizing hemodynamics, which includes allowing a higher blood pressure (ie, permitting mean arterial pressure to reach 90-100 mm Hg), preventing fever, and administering steroids and osmotic diuretics (such as mannitol). Postoperative renal dysfunction is another major concern, particularly in patients with preoperative renal insufficiency, renal arterial disease, or both, so we carefully monitor urine output and serum creatinine levels throughout the postoperative period. When patients begin exhibiting signs of declining renal function, we adjust medications accordingly and liberalize blood pressure control to allow higher mean arterial pressures. To minimize the risk of prosthetic graft infection—another potentially fatal complication of DTA and TAAA repair—we administer antibiotics throughout the postoperative course. Intravenous antibiotics are continued until all drains, chest tubes, and central venous lines are removed.
Long-Term Management Imaging surveillance is an important component of longterm postoperative care after DTA and TAAA repair. All patients remain at risk for subsequent aneurysm formation in their remaining native aortic segments (including reattachment patches) or pseudoaneurysm formation at suture lines as the aorta progressively weakens. Patients should undergo at least annual computed tomographic or magnetic resonance imaging scans of the chest and abdomen to detect complications.
Conclusion For the foreseeable future, open operative procedures for the repair of DTAs and TAAAs will remain a critical part of the armamentarium of cardiothoracic and vascular surgeons. The evolution of endovascular techniques will not entirely supplant the need for surgeons to maintain their skills and advance development of open techniques. Complex aortic disease, progression of disease, and failure of endovascular techniques (for anatomic reasons or because of device failure) will necessitate open reconstruction as a primary or conversion approach. It is central to the concept of open procedures that the multifactorial nature of organ injury mandates a multimodal approach to organ protection. Consistent with the rationale behind our current strategy, we will continue to develop our treatment approach as additional improvements are devised. No one approach is superior; several other specialist centers have developed different but highly successful approaches. Although different surgical practices use vastly divergent surgical techniques, they share a common goal—to improve patient outcomes by reducing factors associated with ischemic complications.
19 Since thoracic endografts first received US Food and Drug Administration approval in 2005,30 we and other experienced sites have comprehensively endorsed and used endovascular therapies for thoracic aortic disease.31 These potentially minimally invasive treatment strategies can provide the greatest benefit to patients judged to be too high-risk for open operations. Accumulation of follow-up data, development of guidelines for appropriate patient selection, and establishment of mortality and morbidity rates equal to or better than those of open surgical repair must be clearly achieved in order for endovascular therapy to supplant open repair.
Acknowledgment The authors thank Carol P. Larsen, CMI, and Scott A. Weldon, MA, CMI, for their outstanding medical illustrations, and Susan Green, MPH, and Stephen N. Palmer, PhD, ELS, for invaluable editorial support.
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20 15. Safi HJ, Hess KR, Randel M, et al: Cerebrospinal fluid drainage and distal aortic perfusion: reducing neurologic complications in repair of thoracoabdominal aortic aneurysm types I and II. J Vasc Surg 23:223-228, 1996 16. Svensson LG, Hess KR, D’Agostino RS, et al: Reduction of neurologic injury after high-risk thoracoabdominal aortic operation. Ann Thorac Surg 66:132-138, 1998 17. Cheung AT, Pochettino A, Guvakov DV, et al: Safety of lumbar drains in thoracic aortic operations performed with extracorporeal circulation. Ann Thorac Surg 76:1190-1196, 2003 18. Dardik A, Perler BA, Roseborough GS, et al: Subdural hematoma after thoracoabdominal aortic aneurysm repair: an underreported complication of spinal fluid drainage? J Vasc Surg 36:47-50, 2002 19. Settepani F, van Dongen EP, Schepens MA, et al: Intracerebellar hematoma following thoracoabdominal aortic repair: an unreported complication of cerebrospinal fluid drainage. Eur J Cardiothorac Surg 24:659-661, 2003 20. Wong DR, Coselli JS, Amerman K, et al: Delayed spinal cord deficits after thoracoabdominal aortic aneurysm repair. Ann Thorac Surg 83: 1345-1355, 2007 21. Griepp RB, Griepp EB: Spinal cord perfusion and protection during descending thoracic and thoracoabdominal aortic surgery: the collateral network concept. Ann Thorac Surg 83:S865-869, 2007 22. Bavaria JE, Woo YJ, Hall RA, et al: Retrograde cerebral and distal aortic perfusion during ascending and thoracoabdominal aortic operations. Ann Thorac Surg 60:345-352, 1995 23. Schepens MA, Vermeulen FE, Morshuis WJ, et al: Impact of left heart bypass on the results of thoracoabdominal aortic aneurysm repair. Ann Thorac Surg 67:1963-1967, 1999
J.S. Coselli and S.A. LeMaire 24. Köksoy C, LeMaire SA, Curling PE, et al: Renal perfusion during thoracoabdominal aortic operations: cold crystalloid is superior to normothermic blood. Ann Thorac Surg 73:730-738, 2002 25. Svensson LG: An approach to spinal cord protection during descending or thoracoabdominal aortic repairs. Ann Thorac Surg 67:1935-1936, 1999 26. Svensson LG, Coselli JS, Safi HJ, et al: Appraisal of adjuncts to prevent acute renal failure after surgery on the thoracic or thoracoabdominal aorta. J Vasc Surg 10:230-239, 1989 27. Hassoun HT, Miller CC III, Huynh TT, et al: Cold visceral perfusion improves early survival in patients with acute renal failure after thoracoabdominal aortic aneurysm repair. J Vasc Surg 39:506-512, 2004 28. Cambria RP, Davison JK, Zannetti S, et al: Thoracoabdominal aneurysm repair: perspectives over a decade with the clamp-and-sew technique. Ann Surg 226:294-303, 1997 29. Etz CD, Di Luozzo G, Bello R, et al: Pulmonary complications after descending thoracic and thoracoabdominal aortic aneurysm repair: predictors, prevention, and treatment. Ann Thorac Surg 83:S870-876, 2007 30. Cho JS, Haider SE, Makaroun MS: US multicenter trials of endoprostheses for the endovascular treatment of descending thoracic aneurysms. J Vasc Surg 43 Suppl A:12A-19A, 2006 31. Lin PH, El Sayed HF, Kougias P, et al: Endovascular repair of thoracic aortic disease: overview of current devices and clinical results. Vascular 15:179-190, 2007