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C. C. Miller et al. Chapter 13 Distal Aortic Perfusion and Selective Visceral Perfusion
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immediate postoperative renal function. The distal ana­stomosis is completed at the iliac bifurcation, using 3-0 or 2-0 polypropylene sutures (Fig. 13.7 f). Prior to the completion of this anastomosis, we place the patient in the head-down position, and then flush the graft proxi­mally and distally. When the anastomosis is completed, we release the clamp to restore pulsatile flow to the low­er extremities.
When the distal extent of the aneurysm is below the renal arteries, the infrarenal abdominal aorta is clamped distally, if possible for the final anastomosis. Sometimes because of excessive aortic calcification or an overly large aorta, we clamp the left common iliac or external iliac artery. The reason for clamping the infra­renal or the left common or external iliac artery is that cooling of the kidneys and viscera can cause the pa­tient's body temperature to drop precipitously, causing cardiac arrhythmias. Core body temperature is kept be­tween 32 and 33 8C by warming the lower extremities. Alternatively, we stop the pump, open the infrarenal ab­dominal aorta and promptly sew the graft to the ab­dominal aorta above the iliac bifurcation. Once the dis­tal anastomosis is completed, we clamp the graft and restart the pump. Pulsatile flow is promptly restored to the legs with completion of the final anastomosis, and the pump is restarted to continue warming the patient to a nasopharyngeal temperature of 36±37 8C. A repre- sentative example of an extent II thoracoabdominal aor­tic aneurysm repair is shown in Fig. 13.8.
13.3 Impact of Adjuncts on Outcome
Between 1991 and 2004, we performed repair of the descending thoracic and thoracoabdominal aorta in 1,106 patients [24]. Seven hundred five (64%) patients were men. The patient distribution was 215 (19.5%) for extent II and 891 (80.5%) for all others. The median age of all patients was 68 years (range, 8±92 years). Three hundred fifty-five (32%) patients were active smokers at the time of surgery. One hundred and eigh­teen (11%) patients suffered from cerebrovascular dis­ease. Forty-five (4%) patients presented with acute dis­section; 73 (6.6%) with rupture [25]. The adjuncts dis­tal aortic perfusion and CSF drainage with moderate hypothermia were used in 823/1,106 (74%) patients. Four hundred thirty-six of 1,106 (39.4%) patients un­derwent intercostal artery reattachment. The overall 30­day mortality was 162/1,106 (14.6%) [25], and the 5­year survival rate was between 60 and 70%. Seventy percent of the patients recover from surgery without postoperative complications. Risk factors for mortality were advanced age, renal failure and paraplegia [26]. Remarkably, the use of adjunct distal aortic perfusion and CSF drainage was found to provide a beneficial ef­fect on long-term survival (Fig. 13.9).
Fig. 13.9. Kaplan±Meier actuarial plot showing the beneficial
10-year survival effect of adjunct distal aortic perfusion and cerebrospinal fluid drainage (yellow line) compared with no adjunct (red line)
13.3.1 Neurological Deficit: Immediate and Delayed
In our cumulative experience, neurological deficit has been reduced by 3.7-fold with the combined adjunct distal aortic perfusion and CSF drainage [26]. The inci­dence of neurological deficit for all patients without the use of adjunct was 5.7%, and 2.4% with adjunct. Aortic cross-clamp times have increased significantly since 1991, yet the rate of neurologic deficit has declined in that time. Although other previously established risk factors remain significantly associated with neurologic deficit, aortic cross-clamp time is no longer associated to neurologic deficit (Fig. 13.10a,b). In the high-risk ex­tent II, adjuncts reduced neurological deficit from 21 to
3.3% [24]. Clearly, the adoption of adjunct has im­pacted the overall incidence of neurological deficit, and this has led us to redefining the low versus high risk, as extent ªnon-IIº versus extent II.
Interestingly, as improved spinal cord protection dur­ing thoracoabdominal aortic surgery has reduced the overall incidence of neurological complications, de­layed-onset neurological deficit (the onset of paraplegia or paraparesis after a period of observed normal neuro­logical function) has emerged as a significant clinical entity [2, 28]. We have observed delayed neurological deficit as early as 2 h and as late as 2 weeks following surgery. The exact mechanisms involved in the develop­ment of delayed neurological deficit remain unknown. However, we speculate that delayed neurological deficit after thoracoabdominal aortic repair may result from a ªsecond hitº phenomenon [29]. That is, although ad­juncts can protect the spinal cord intraoperatively and reduce the incidence of immediate neurological deficit, the spinal cord is still ªvulnerableº during the early
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III. Treatment of Thoracic Degenerative Aortic Aneurysms
a
with delayed neurological deficits. In exploring other possible causes of delayed neurological deficit we have found no outstanding single risk factor. Using multi­variable analyses, however, we have identified acute dis­section, extent II and renal insufficiency as significant preoperative predictors for delayed-onset neurological deficit [30]. Postoperative clinical predictors of delayed neurological deficit include hemoglobin level less than 9 g/dL, mean arterial pressure less than 90 mmHg and CSF drain complications [31].
To optimize postoperative spinal cord perfusion and oxygen delivery, we keep the mean arterial pressure above 90±100 mmHg, hemoglobin above 10 mg/dL and cardiac index greater than 2.0 L/min. If delayed neuro­logical deficit occurs, measures to increase spinal cord perfusion are instituted immediately. The patient is placed flat in the supine position and patency and func­tion of the drain is ascertained at once. If the drain has been removed, the CSF catheter is reinserted immedi­ately and CSF is drained freely until the CSF pressure drops below 10 mmHg. The systemic arterial pressure is raised, blood transfusion is liberally infused and oxygen saturation is increased, as indicated earlier. CSF drain­age is continued for at least 72 h for all patients with delayed-onset neurological deficit. Using this approach, we have seen improvement in neurological function in 57% of our patients [30]. Patients who developed de­layed neurological deficit but did not have CSF drainage failed to recover function.
b
Fig. 13.10. Multiple logistic regression analyses according to
risk of neurologic deficit and cross-clamp time without (a) and with (b) adjunct use
postoperative period. Additional ischemic insults, such as hemodynamic instability or malfunction of the CSF drainage catheter, may constitute a second hit, causing delayed neurological deficit. Furthermore, in the rigid unyielding spinal column, any rise in CSF pressure could lead to an increase in compartment pressure, with consequent decreased spinal cord perfusion. Hence, our reason for intermittent perioperative CSF drainage is to maintain the compartment pressure be­low 10 mmHg, and the same rationale applies to our approach using continuous CSF drainage in patients
13.3.2 Renal Failure
We have used and appraised many different forms of re­nal protection. including distal aortic perfusion, warm blood visceral perfusion, antegrade cold blood visceral perfusion, retrograde cold blood perfusion and the perioperative use of a renal protective pharmacologic agent, fenoldopam. None of these yielded overly prom­ising results. Using multivariable analyses, we found preoperative renal failure (creatinine above 2.8 g/dL), left renal artery reattachment, visceral perfusion and clamp-and-go technique as predictors of acute renal failure [32]. In the past, we had used visceral perfusion without cooling and without systemic heparin, and this was likely the reason for the negative effect of visceral perfusion on renal protection. We recently reviewed the impact of various adjuncts on renal function. Distal aortic perfusion has emerged as protective, but only for aortic repair that does not directly involve the renal ar­teries. There is evidence, however, that patients treated with cold blood visceral perfusion have superior surviv­al and recovery rates, and this may be related to im­proved liver protection. None of the adjuncts thus far evaluated have clearly prevented acute renal failure. The major predictors of postoperative renal dysfunction re-
C. C. Miller et al. Chapter 13 Distal Aortic Perfusion and Selective Visceral Perfusion
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main preoperative renal function, cross-clamp time and repair extending to the renal arteries. In our cumulative experience of descending thoracic and thoracoabdom­inal aortic repairs, we found that acute renal failure oc­curred in 17.8% of our patients overall. The incidence for descending thoracic repairs was 7.2% and 22.8% for thoracoabdominal aortic repairs. Thirty-day mortality among patients with acute renal failure was 30% com­pared with 10% mortality for all other patients. Although we had theorized that patients with the most extensive thoracoabdominal aortic aneurysm (extent II) would be at highest risk for the development of postop­erative renal failure, multivariable analyses did not find aneurysm extent to be a significant predictor. Approxi­mately one third of our patients who developed acute renal failure remained on hemodialysis, and long-term survival for patients on hemodialysis has been dismal.
13.3.3 Aortic Dissection
a
During the clamp-and-go era, aortic dissection was considered a risk factor for neurological deficit in pa­tients undergoing surgery of the thoracoabdominal aor­ta [18]. With the use of distal aortic perfusion and CSF drainage, however, chronic dissection no longer poses a threat [33]. We recently showed similar low rates of paraplegia for patients who received adjuncts when un­dergoing thoracoabdominal aortic surgery, whether they had aortic dissection or not, 3.6% versus 4.7%, respec­tively. However, various surgical technical modifications are required in repairing dissected thoracoabdominal aorta, particularly in the acute phase. Identification of the true versus the false lumen is imperative. The parti­tion/septum between the two lumens is excised (Fig. 13.11 a). Before sewing the graft, we usually rein­force both proximal and distal ends of the dissected aorta with a running 4-0 polypropylene suture. Addi­tional interrupted pledgeted polypropylene sutures are then placed in the posterior and anterior walls for further reinforcement (Fig. 13.11b). Whereas we always attempt to reattach patent lower intercostal arteries dur­ing graft replacement of the descending thoracic and thoracoabdominal aorta, we advocate ligation of all pat­ent intercostal and lumbar arteries in the acutely dis­sected aorta, to avoid catastrophic bleeding associated with the friable tissues. Patent lower intercostal arteries can be safely reattached in chronic dissection using our described technique. In general, we replace all aneurys­mal aortic segments, but leave the nonaneurysmal seg­ment even if dissected.
b
Fig. 13.11. Illustration of a thoracoabdominal aortic aneurysm
repair showing excision of the distal partition/septum between the true and false lumens, and completed graft replacement with reinforced anastomoses
13.4 Summary
149
Incredible progress has been made in the treatment of thoracoabdominal aortic aneurysms since its inception. The various strategies of organ protection including the use of distal aortic perfusion, CSF drainage, visceral
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III. Treatment of Thoracic Degenerative Aortic Aneurysms
perfusion, sequential aortic cross-clamp, intercostal ar­tery reattachment and moderate hypothermia, as well as the evolution of surgical approach have all contribut­ed to the decline in mortality and morbidity. Our re­fined surgical techniques and use of adjuncts have re­duced the overall incidence of neurological deficits fol­lowing thoracoabdominal aortic aneurysm repair to
2.4%, and to 6.6% for patients with extent II. Our con­tinuing goals are to further decrease the incidence of neurological deficits and to improve renal protection, with particular focus on the extent II thoracoabdominal aortic aneurysm.
Acknowledgement. We are grateful to Carl Clingman for
his illustrative and photographic contributions and to Kirk Soodhalter for his editorial assistance.
References
1. Etheredge S, Yee J, Smith J, et al. Successful resection of a large aneurysm of the upper abdominal aorta and replace­ment with homograft. Surgery 1955; 138:1071±1081.
2. De Bakey ME, Creech O Jr, Morris GC Jr. Aneurysm of the thoracoabdominal aorta involving the celiac, mesen­teric and renal arteries. Report of four cases treated by re­section and homograft replacement. Ann Surg 1956; 179:763±772.
3. Matas R. An operation for the radical cure of aneurysm based upon arteriorrhaphy. Ann Surg 1903; 37:161±196.
4. Carrell A. Results of the transplantation of blood vessels, organs and limbs. JAMA 1908; 51:1662±1667.
5. Creech O Jr. Endo-aneurysmorrhaphy and treatment of aortic aneurysm. Ann Surg 1966; 164:935±946.
6. Connolly JE, Wakabayashi A, German JC, Stemmer EA, Serres EJ. Clinical experience with pulsatile left heart by­pass without anticoagulation for thoracic aneurysms. J Thorac Cardiovasc Surg 1971; 62:568±576.
7. Korompai F, Hayward R. Preservation of visceral perfu­sion during resection of thoracoabdominal aortic aneu­rysm. Cardiovasc Dis Bull Tex Heart Inst 1975; 2:349.
8. Crawford ES. Thoraco-abdominal and abdominal aortic aneurysms involving renal, superior mesenteric, celiac ar­teries. Ann Surg 1974; 179:763±772.
9. Cunningham JN Jr, Laschinger JC, Merkin HA, et al. Mea­surement of spinal cord ischemia during operations upon the thoracic aorta: initial clinical experience. Ann Surg 1982; 196:285±296.
10. Laschinger JC, Cunningham JN J, Nathan IM, Knopp EA, Cooper MM, Spencer FC. Experimental and clinical as­sessment of the adequacy of partial bypass in mainte­nance of spinal cord blood flow during operations of the thoracic aorta. Ann Thorac Surg 1983; 36:417±426.
11. Crawford ES, Mizrahi EM, Hess KR, Coselli JS, Safi HJ, Patel VM. The impact of distal aortic perfusion and so­matosensory evoked potential monitoring on prevention of paraplegia after aortic aneurysm operation. J Thorac Cardiovasc Surg 1988; 95:357±367. Erratum in: J Thorac Cardiovasc Surg 1989; 97:665.
12. McCullough J, Hollier L, Nugent M. Paraplegia after thor­acic aortic occlusion: influence of cerebrospinal fluid drainage. Experimental and early clinical results. J Vasc Surg 1988; 7:153±160.
13. Crawford ES, Svensson LG, Hess KR, et al. A prospective randomized study of cerebrospinal fluid drainage to pre­vent paraplegia after high-risk surgery on the thoracoab­dominal aorta. J Vasc Surg 1991; 13:36±45; discussion 45±
46.
14. Crawford ES, Crawford JL, Safi HJ, et al. Thoracoabdom­inal aortic aneurysms: preoperative and intraoperative factors determining immediate and long-term results of operations in 605 patients. J Vasc Surg 1986; 3:389±404.
15. Crawford ES, Coselli JS, Safi HJ. Partial cardiopulmonary bypass, hypothermic circulatory arrest, and posterolateral exposure for thoracic aortic aneurysm operation. J Thorac Cardiovasc Surg 1987; 94:824±827.
16. Kouchoukos NT, Daily BB, Rokkas CK, Murphy SF, Bauer S, Abboud N. Hypothermic bypass and circulatory arrest for operations on the descending thoracic and thoracoab­dominal aorta. Ann Thorac Surg 1995; 60:67±76; discus­sion 76±77.
17. Cambria R, Davison J, Zannetti S, et al. Clinical experi­ence with epidural cooling for spinal cord protection dur­ing thoracic and thoracoabdominal aneurysm repair. J Vasc Surg 1997; 25:241±243.
18. Svensson LG, Crawford ES, Hess KR, Coselli JS, Safi HJ. Experience with 1509 patients undergoing thoracoabdom­inal aortic operations. J Vasc Surg 1993; 17:357±368; dis­cussion 368±370.
19. 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 1996; 23:223±228; discus­sion 229.
20. Safi HJ, Bartoli S, Hess KR, et al. Neurologic deficit in pa­tients at high risk with thoracoabdominal aortic aneu­rysms: the role of cerebral spinal fluid drainage and distal aortic perfusion. J Vasc Surg 1994; 20:434±444; discussion 442±443.
21. Engle J, Safi HJ, Miller CC 3rd, et al. The impact of dia­phragm management on prolonged ventilator support after thoracoabdominal aortic repair. J Vasc Surg 1999; 29:150±156.
22. Huynh TT, Miller CC 3rd, Estrera AL, Sheinbaum R, Allen SJ, Safi HJ. Determinants of hospital length of stay after thoracoabdominal aortic aneurysm repair. J Vasc Surg 2002; 35:648±653.
23. Safi H, Miller CI, Carr C, Illiopoulos D, Dorsay D, Bald­win J. The importance of intercostal artery reattachment during thoracoabdominal aortic aneurysm repair. J Vasc Surg 1998; 27:58±68.
24. Safi HJ, Estrera AL, Miller CC 3rd, Huynh TT, Porat EE, Azizzadeh A, Meada R, Goodrick JS. Evolution of risk for neurologic deficit after descending and thoracoabdominal aortic repair. Ann Thorac Surg 2005; 80:2173±2179.
25. Huynh TT, van Eps RG, Miller CC 3rd, Villa M, Estrera AL, Azizzadeh A, Porat EE, Goodrick JS, Safi HJ. Evolu­tion of risk for neurologic deficit after descending and thoracoabdominal aortic repair. J Vasc Surg 2005; 42:206±
212.
26. Safi HJ, Miller CC 3rd, Huynh TTT, et al. Distal aortic perfusion and cerebrospinal fluid drainage for thoracoab­dominal and descending thoracic aortic repair: Ten years of organ protection. Ann Surg 2003; 238:372±381.
27. Safi HJ, Miller CC 3rd, Azizzadeh A, Iliopoulos DC. Ob­servations on delayed neurologic deficit after thoracoab­dominal aortic aneurysm repair [see comments]. J Vasc Surg 1997; 26:616±622.
28. Azizzadeh A, Huynh TT, Miller CI, Safi H. Reversal of twice-delayed neurologic deficits with cerebrospinal fluid drainage after thoracoabdominal aneurysm repair: a case report and plea for a national database collection. J Vasc Surg 2000; 31:592±598.
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29. Huynh TT, Miller CC 3rd, Safi HJ. Delayed onset of neu­rologic deficit: significance and management. Semin Vasc Surg 2000; 13:340±344.
30. Estrera AL, Miller CC 3rd, Huynh TT, Azizzadeh A, Porat EE, Vinnerkvist A, Ignacio C, Sheinbaum R, Safi HJ. Pre­operative and operative predictors of delayed neurologic deficit following repair of thoracoabdominal aortic aneu­rysm. J Thorac Cardiovasc Surg 2003; 126:1288±1294.
31. Azizzadeh A, Huynh TTT, Miller CC 3rd, et al. Postopera­tive risk factors for delayed neurologic deficit after thor-
acic and thoracoabdominal aortic aneurysm repair: a case-control study. J Vasc Surg 2003; 37:750±754.
32. Safi HJ, Harlin SA, Miller CC, et al. Predictive factors for acute renal failure in thoracic and thoracoabdominal aor­tic aneurysm surgery. J Vasc Surg 1996; 24:338±344; dis­cussion 344±345. Erratum in: J Vasc Surg 1997; 25:93.
33. Safi HJ, Miller CC 3rd, Estrera AL, et al. Chronic aortic dissection not a risk factor for neurologic deficit in thora­coabdominal aortic aneurysm repair. Eur J Vasc Endovasc Surg 2002; 23:244±250.
Femoral Bypass and Hypothermia
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for the Treatment of Thoracoabdominal Aneurysms
R. Scott Mitchell
Chapter
14
Contents
14.1 Introduction ......................
14.2 Operative Strategies .................. 153
14.3 Methods .........................154
153
14.1 Introduction
Aneurysms of the descending thoracic and thoracoab­dominal aorta range from focal outpouchings of the thoracic aorta to extensive degenerative aneurysms en­compassing the entire thoracoabdominal aorta. Similar­ly, treatment strategies range from simple clamp tech­niques, unsupported by distal perfusion, the ªclamp­and-goº technique, to more complex techniques utiliz­ing distal perfusion, separate visceral perfusion, and hy­pothermia as an adjunct for preservation of spinal cord function. This treatise advances our rationale for a more aggressive perfusion strategy that affords optimal protection for CNS, spinal cord, and abdominal viscera.
Although the simplicity of a clamp-and-go approach is attractive, there are severe perturbations that argue against its utility. Proximal clamping of the descending thoracic aorta or distal arch presents several major dif­ficulties. First, in many instances with diffuse atheroma­tous change, clamping of the distal arch may be unsafe, with central embolization of atheromatous debris into the cerebral vasculature. Second, proximal clamping may not afford sufficient normal proximal aorta to al­low a secure proximal anastomosis. Third, proximal clamping also produces severe hemodynamic distur­bances, including proximal hypertension, an abrupt in­crease in afterload, a decrease in distal perfusion pres­sure, and an increase in cerebrospinal fluid (CSF) pres­sure [1]. In addition to a profound sympathetic stimula­tion, there is also requisite distal ischemia, with second­ary and injurious metabolic changes, increasing the likelihood for spinal cord and visceral end-organ injury. Similarly, with the release of the aortic cross-clamp, further hemodynamic perturbations are again pro-
duced, many of which will aggravate a previous insult, including proximal hypotension, washout of ischemic metabolites, and reperfusion injury, all compounding the effects of the prior ischemic injury.
Distal aortic perfusion techniques may substantially reduce many of these ill effects, albeit at the price of in­troducing negative attributes essential for extracorpore­al perfusion, including anticoagulation, stimulation of the inflammatory response, and alterations in coagula­tion.
In the absence of distal aortic perfusion, the tech­nique of simple aortic clamping is limited to a ªsafe ischemic period,º unpredictable, and likely highly vari­able for different vascular beds. Historically, spinal cord complications have been noted to rise significantly after 30±35 min of ischemia, with similar end-organ dysfunc­tion becoming apparent after slightly longer ischemic intervals for kidneys and liver. In an effort to minimize these secondary perturbations, distal perfusion tech­niques have been developed to allow longer periods of ischemia and more complex reconstructions [2]. It is our contention that femoral±femoral bypass provides a stable operative environment, facilitates surgical recon­struction, provides good end-organ preservation, and affords valuable flexibility for improved surgical results, with only modest negative repercussions.
14.2 Operative Strategies
A thorough preoperative assessment, including physical examination, assessment of physiologic cardiac, pulmo­nary, and renal reserve, and scrutiny of available imag­ing modalities precedes operative intervention. Surgical as well as perfusion strategies are then decided.
The major downside of femoral±femoral bypass is the necessity for full heparinization as a membrane oxygenator is an integral part of the perfusion circuit. Usually 300 IU/kg is sufficient to maintain an activated clotting time of more than 400 s. Fully heparin coated circuitry may allow a lower systemic heparin level, usually 100 IU/kg heparin and an activated clotting
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III. Treatment of Thoracic Degenerative Aortic Aneurysms
time of more than 180 s. Although expensive, fully coated circuitry may be associated with less blood loss, reduced transfusion requirements, and perhaps a de­crease in the systemic inflammatory response. Similarly, the use of aprotinen (Trasolol, Bayer Pharmaceuticals) has been associated with decreased blood loss and a de­creased requirement for transfusion products, but re­quires ascertainment of adequate heparin effect, namely a Kaolin-determined activated clotting time of more than 400 s, and a heparin concentration of more than
3.5 mg/kg. The major advantage of femoral±femoral bypass is
flexibility. For thoracic or thoracoabdominal aneurysms in which the distal arch is unsuitable for clamping (large diameter, severe calcification, intraluminal atherogenic debris, proximal extension of dissection flap), hypothermic circulatory arrest (HCA) is the method of choice for constructing a secure proximal anastomosis and avoiding cerebral atheroembolic injury. Similarly, for patients in whom sequential cross-clamp­ing of the aorta is not possible (chronic dissection, large mural thrombus, or generalized aneurysmal en­largement without focal narrowing), HCA is an excel­lent method of spinal cord protection, coupled with dis­tal aortic perfusion and CSF drainage [3±5]. The oxy­genator also adds flexibility, such as with the patient with poor oxygenation who may become a ventilatory problem during single lung ventilation.
14.3 Methods
Preoperatively, an epidural catheter and a CSF drain are placed prior to operative intervention. Full intraopera­tive monitoring is employed, including radial and femo­ral artery pressure monitoring, large-bore intravenous access, and transesophageal echo (TEE). A double-lu­men endotracheal tube facilitates operative exposure and minimizes operative trauma to the left lung. Both femoral arterial and venous access are attained via an oblique supra-inguinal crease incision.
Long, flexible, thin-walled venous catheters are avail-
able with tapered over-the-wire dilators that almost uni­formly assure access to the right atrium. Endovascular access through the femoral vein can be ascertained by TEE visualization of the guide wire emerging from the inferior vena cava, traversing the right atrium, and en­tering the superior vena cava. If passage of a soft ªJº­tipped guide wire is not successful, a floppy-tip Glide­wire (Terumo, Tokyo, Japan) and a Benson catheter fre­quently assure passage.
Arterial cannulation is either via a transverse arter-
iotomy with a 22-F arterial catheter, or over a guide wire using a 17-F or a 19-F catheter (DLP).
Successful cannulation is assured by easy aspiration
of venous blood from the venous catheter, and pulsatile
flow from the arterial catheter with a pulsatile wave form in the cardiopulmonary bypass pump circuitry.
Full thoracoabdominal exposure is attained in the routine manner. Proximally, the distal arch and proxi­mal descending thoracic aorta are circumferentially dis­sected, with careful sharp dissection of the phrenic, va­gus, and recurrent laryngeal nerves. After careful palpa­tion, inspection, and perhaps interrogation by transeso­phageal echocardiography, and/or epiaortic ultrasound, a decision is made whether the aorta can be safely clamped to allow a secure proximal anastomosis. If not, femoral±femoral bypass is used to cool the patient to 16±18 8C, and an open proximal anastomosis is con­structed to the full-thickness divided aorta of normal caliber. Great care is taken to prevent any atheromatous debris from falling into the dependent aortic arch, and retrograde cerebral perfusion through the long venous cannula can be used as a partial flush of the arch ves­sels. Following completion of the anastomosis, the new graft is cannulated and clamped distally, and retrograde arterial perfusion of the heart and great vessels is re­sumed.
If retrograde perfusion from the femoral artery is thought to entail significant risk for retrograde emboli­zation, separate antegrade cerebral perfusion can be performed from a previously placed 6-mm Dacron side limb sewn to the left common carotid artery established prior to thoracotomy.
If the aorta is focally narrowed so as to allow se­quential cross-clamping, then that is done serially down the aorta, allowing retrograde femoral perfusion to pro­vide visceral perfusion until that aortic segment is opened. Initially, a distal clamp at mid-chest allows ret­rograde perfusion of critical intercostal arteries. Then, clamping just above the celiac axis allows identification of large paired intercostals at the T8±T12 level which need to be attached to the graft. Decision-making about which arteries to reattach is guided by the identification of the anterior spinal artery on computed tomography or magnetic resonance imaging [6, 7], loss of either evoked sensory or motor potentials, and by their gener­al suitability at the time of operation. It should be noted that while hypothermia is an excellent adjunct for spinal cord protection, it also effectively silences neural response, thus limiting the utility of either evoked sen­sory or motor potentials.
After attachment of the intercostal artery pairs, at­tention is directed toward the visceral vessels, which are now individually cannulated with balloon-tipped perfu­sion catheters and perfused with cold blood. Depending on the local anatomy, and the quality of this portion of the aorta, this reconstruction may utilize the island technique, frequently incorporating the celiac axis, su­perior mesenteric artery, and right renal artery as one button, and the left renal artery as a second button. Al­ternatively, if the quality of the aortic tissues is poor, individual grafts may be led separately to each visceral
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vessel orifice. Preloading short Dacron graft segments on the balloon catheters prior to initiating perfusion greatly facilitates this reconstruction, and minimizes visceral ischemic time.
Distally, after exposure of the aorta in the retroperi­toneal plane, the distal end point is determined, and the aorta is again circumferentially dissected.
Again, if this can be safely clamped, and a secure anastomosis obtained, then distal aortic perfusion is used distal to the aortic clamp. If a satisfactory length of normal aorta is not available, then distal perfusion is temporarily discontinued, and an open distal full-thick­ness anastomosis is constructed.
The beauty of hypothermia is that it allows the safe conduct of these multiple previous maneuvers for all patients, regardless of the extent of aortic disease, and without the risk of atheroembolization. Cardiopulmo­nary bypass is initiated, and the proximal and distal dissection completed while cooling proceeds to 16± 188C, with assurance of EEG silence. After equilibration of a core temperature of 16±18 8C for at least 5 min, car- diopulmonary bypass is discontinued in the head-down position, and retrograde perfusion through the venous catheter is commenced at approximately 500 ml/min to continuously flush the cerebral vasculature. The aneu­rysm is incised to the level of the renal arteries, and visceral artery perfusion is instigated with balloon­tipped catheters. The proximal aorta is transected to al­low construction of a full-thickness anastomosis to nor­mal aorta, after which the graft is then cannulated, clamped distally, and retrograde arterial perfusion es­tablished to cardiac and brachiocephalic vessels. Next, selective intercostal artery reimplantation is effected to large patent intercostal arteries in the critical zone. Pre­operative localization of contributing intercostal pairs to the anterior spinal artery can be obtained with com­puted tomographic or magnetic resonance imaging. Ex­cellent spinal cord protection is afforded during this in­terval by generalized hypothermia and perfusion of col­laterals from the left vertebral and hypogastric systems.
The paravisceral aorta is then assessed. For good­quality aorta in the absence of connective tissue disease, aortic island reconstruction is effected, usually with the celiac axis, superior mesenteric artery, and right renal artery as one island, and the left renal artery as a sepa­rate full-thickness button. Alternatively, especially for Marfan patients in whom aneurysmal dilation of the visceral island has been noted, individual branch vessel reconstruction with 6-, 8-, or 10-mm Dacron grafts can be accomplished during continuous perfusion via bal­loon-tipped catheters. An open distal anastomosis is then completed, allowing restoration of femoral perfu-
sion after clamping of the graft. Individual visceral branch vessel grafts can then be reimplanted into the central aorta graft between clamps, allowing continuous perfusion of cardiac, cerebral, and intercostal arteries, and pelvic circulation during reimplantation and warm­ing. Visceral ischemic time is limited to the time neces­sary to reimplant Dacron side limbs into a central aor­tic graft, and its effect is minimized by the now regional hypothermia.
Although full heparinization is necessary, cardiac, central nervous system, and spinal cord protection is assured, and the hepatic contribution to postoperative coagulation is preserved by hypothermia and continu­ous perfusion.
Although there is a requirement for full hepariniza­tion in order to use an oxygenator, this coagulopathy may be more than offset by avoiding the use of rein­fused washed red cells, with their own inherent coagu­lopathic tendencies. Integrity of all anastomoses can be easily assured during the period of rewarming, and the patient can then be weaned from cardiopulmonary by­pass. Although a somewhat prolonged cardiopulmonary bypass run may be necessary, especially in the obese patient, good end-organ preservation is assured, and the risk of atheroembolism minimized. With more tar­get-specific anticoagulation, coagulopathies secondary to a prolonged cardiopulmonary bypass run can be minimized, and excellent end-organ preservation can be achieved by these techniques.
References
1. Gelman S. The pathophysiology of aortic cross-clamping
and unclamping. Anesthesiology 1995; 82:1026±1060.
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Branch Stent-Graft Systems and
https://t.me/med1917
Less Invasive Combined Surgical and Endovascular Treatment for Descending Thoracic Aortic Aneurysms
Krassi Ivancev, Bansi Koul
Chapter
15
Contents
15.1 Introduction ......................
15.2 Elongation of the Landing Zone
intheAorticArch ...................
15.3 Total Arch Replacement
with Open Stent-Graft Placement ..........
15.4 Branch Stent-Grafts
fortheThoracicAorticArch .............
15.5 Discussion ........................ 159
157
157
158
159
15.1 Introduction
Endovascular aneurysm repair (EVAR) in the thoracic aorta has repeatedly been shown to offer advantages over open surgery thanks to its less traumatic nature. However, EVAR is limited by the absolute requirement of an adequate landing zone at least 15 mm in length in order to provide successful exclusion of an aneurysm or a dissection. In addition, the landing zone may need to be even longer when it comes to aneurysms and/or dis­sections in the aortic arch, where currently available stent-grafts do not provide an effective hemostatic seal owing to their relatively high rigidity [1]. For these pa­tients, the alternative is conventional total aortic arch replacement using hypothermic extracorporeal circula­tion, which, in spite of recent improvements, continues to be associated with considerable mortality and the risk of cerebral complications, especially in patients with severe comorbidities. Therefore, combining the ad­vantages of EVAR and various types of open vascular surgery may offer a valuable alternative for this catego­ry of patients.
15.2 Elongation of the Landing Zone in the Aortic Arch
In patients with symptomatic type B dissections or an­eurysms in the aortic arch, it is not uncommon to cover the left subclavian artery as a means of prolonging the landing zone and thereby achieving a secure hemostatic seal for a stent-graft. However, such a maneuver may not be sufficient. The stent-graft may need to be placed further cephalad and may cover the left carotid artery as well. In order to provide continuous flow to the blocked vessels an extraanatomic bypass from the inno­minate artery to the left carotid and left subclavian ar­teries may be performed. Such a technique has been shown to be safe and efficient [2]. Occasionally, though, currently available stent-grafts may not line up along a severely angulated aortic arch with a persistent type I endoleak as a result [1]. Under these circumstances it may be advisable to place a band of Teflon felt around the aortic arch once the stent-graft is in place (Fig. 15.1). This is achieved through a minimal median sternotomy. The same access may also be used for su­praaortic transposition with a bi- or trifurcated graft originating from the ascending aorta and anastomosing to the innominate artery, the left carotid artery, and the left subclavian artery [3, 4]. This is achieved without hypothermic cardiopulmonary arrest and using a side­clamp in the ascending aorta. With such an approach the trauma is kept to a minimum, avoiding total arch replacement or left thoracotomy. If a bypass is per­formed to the innominate artery the stent-graft may be extended across the origin of all the supraaortic vessels (Fig. 15.2).
158
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III. Treatment of Thoracic Degenerative Aortic Aneurysms
a
b
c
Fig. 15.1. a Schematic drawing representing placement of a
band distal to the left subclavian artery in order to create a se­cure implantation site for a stent-graft. placement of the stent-graft showing indentation from the band placed in the aortic arch. ment of the stent-graft showing a good hemostatic seal.
d Computed tomography (CT) 6 months after stent-graft place-
ment showing a well-excluded aneurysm
Fig. 15.2. Schematic drawing showing a supraaortic transposi-
tion using a trifurcated graft anastomosed to the ascending aorta and further to the innominate, left carotid, and left sub­clavian arteries. The stent-graft is placed across the aortic arch excluding an aneurysm and a type B dissection
c Aortogram following deploy-
b Aortogram during
d
15.3 Total Arch Replacement with Open Stent-Graft Placement
This technique is recommended when concomitant heart surgery is performed, including coronary bypass, graft replacement with or without aortic valve remodel­ing in the ascending aorta due to aneurysm formation or type A dissection, or when there is a type A dissec­tion continuing into the descending thoracic aorta [5, 6, 7]. In these situations a stent-graft may be placed from the distal aortic arch under hypothermic cardiopulmo­nary arrest and guided either fluoroscopically or by transesophageal echography. The proximal end of the stent-graft is then sutured to the posterior wall of the aorta and possibly attached to a graft used for aortic arch replacement (Fig. 15.3). There is also a possibility to use a ªstented elephant trunkº in the case of an an-