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81. Seeger JM.Management of patients with prosthetic vascular graft infection. Am Surg. 2000;66(2):166–77.
82. Vogel TR, Symons R, Flum DR.The incidence and factors associ­ated with graft infection after aortic aneurysm repair. J Vasc Surg. 2008;47(2):264–9.
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85. Kieffer E, Bahnini A, Koskas F, Ruotolo C, Le Blevec D, Plissonnier D.In situ allograft replacement of infected infrarenal aortic prosthetic grafts: results in forty-three patients. J Vasc Surg. 1993;17(2):349–55. discussion 55-6.
86. Hayes PD, Nasim A, London NJ, Sayers RD, Barrie WW, Bell PR, etal. In situ replacement of infected aortic grafts with rifampicin­bonded prostheses: the Leicester experience (1992 to 1998). J Vasc Surg. 1999;30(1):92–8.
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95. Schurink GW, Peppelenbosch N, Mees B, Jacobs MJ.Diagnostic algorithms and treatment strategies in primary aortic and aortic graft infections. J Cardiovasc Surg. 2016;57(2):224–32.
96. Daenens K, Fourneau I, Nevelsteen A. Ten-year experience in autogenous reconstruction with the femoral vein in the treatment of aortofemoral prosthetic infection. Eur J Vasc Endovasc Surg. 2003;25(3):240–5.
97. Chambers ST.Diagnosis and management of staphylococcal infec­tions of vascular grafts and stents. Intern Med J. 2005;35(Suppl
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98. Hodgkiss-Harlow KD, Bandyk DF. Antibiotic therapy of aor­tic graft infection: treatment and prevention recommendations. Semin Vasc Surg. 2011;24(4):191–8.
99. Garot M, Delannoy PY, Meybeck A, Sarraz-Bournet B, d'Elia P, d'Escrivan T, etal. Intra-abdominal aortic graft infection: prognos­tic factors associated with in-hospital mortality. BMC Infect Dis. 2014;14:215.
100. Qvarfordt PG, Reilly LM, Mark AS, Goldstone J, Wall SD, Ehrenfeld WK, et al. Computerized tomographic assessment of graft incorporation after aortic reconstruction. Am J Surg. 1985;150(2):227–31.
101. Valentine RJ.Diagnosis and management of aortic graft infection. Semin Vasc Surg. 2001;14(4):292–301.
102. Spartera C, Morettini G, Petrassi C, Marino G, Minuti U, Pavone P, etal. Role of magnetic resonance imaging in the evaluation of aortic graft healing, perigraft uid collection, and graft infection. Eur J Vasc Surg. 1990;4(1):69–73.
103. Shahidi S, Eskil A, Lundof E, Klaerke A, Jensen BS.Detection of abdominal aortic graft infection: comparison of magnetic reso­nance imaging and indium-labeled white blood cell scanning. Ann Vasc Surg. 2007;21(5):586–92.
104. Spacek M, Belohlavek O, Votrubova J, Sebesta P, Stadler P.Diagnostics of “non-acute” vascular prosthesis infection using 18F-FDG PET/CT: our experience with 96 prostheses. Eur J Nucl Med Mol Imaging. 2009;36(5):850–8.
105. Lawrence PF, Dries DJ, Alazraki N, Albo D Jr. Indium 111-labeled leukocyte scanning for detection of prosthetic vascular graft infec­tion. J Vasc Surg. 1985;2(1):165–73.
106. Lyons OT, Baguneid M, Barwick TD, Bell RE, Foster N, Homer­Vanniasinkam S, etal. Diagnosis of aortic graft infection: a case def­inition by the Management of Aortic Graft Infection Collaboration (MAGIC). Eur J Vasc Endovasc Surg. 2016;52(6):758–63.
107. Ducasse E, Calisti A, Speziale F, Rizzo L, Misuraca M, Fiorani P.Aortoiliac stent graft infection: current problems and manage­ment. Ann Vasc Surg. 2004;18(5):521–6.
108. Laser A, Baker N, Rectenwald J, Eliason JL, Criado-Pallares E, Upchurch GR Jr. Graft infection after endovascular abdominal aortic aneurysm repair. J Vasc Surg. 2011;54(1):58–63.
109. Sharif MA, Lee B, Lau LL, Ellis PK, Collins AJ, Blair PH, etal. Prosthetic stent graft infection after endovascular abdominal aor­tic aneurysm repair. J Vasc Surg. 2007;46(3):442–8.
110. Ohta T, Hosaka M, Ishibashi H, Sugimoto I, Takeuchi N, Kazui H, etal. Treatment for aortic graft infection. Surg Today. 2001;31(1):18–26.
111. Hobbs SD, Kumar S, Gilling-Smith GL.Epidemiology and diag­nosis of endograft infection. J Cardiovasc Surg. 2010;51(1):5–14.
112. Setacci C, De Donato G, Setacci F, Chisci E, Perulli A, Galzerano G, et al. Management of abdominal endograft infection. J Cardiovasc Surg. 2010;51(1):33–41.
113. May J.Complications of endovascular aortic repair. J Cardiovasc Surg. 2010;51(1):1–3.
114. Samson RH, Veith FJ, Janko GS, Gupta SK, Scher LA.A modi­ed classication and approach to the management of infec­tions involving peripheral arterial prosthetic grafts. J Vasc Surg. 1988;8(2):147–53.
115. Reilly L. Aortic graft infection: evolution in management. Cardiovasc Surg. 2002;10(4):372–7.
116. Brown KE, Heyer K, Rodriguez H, Eskandari MK, Pearce WH, Morasch MD.Arterial reconstruction with cryopreserved human allografts in the setting of infection: a single-center experience with midterm follow-up. J Vasc Surg. 2009;49(3):660–6.
117. Saleem BR, Meerwaldt R, Tielliu IF, Verhoeven EL, van den Dungen JJ, Zeebregts CJ.Conservative treatment of vascular pros­thetic graft infection is associated with high mortality. Am J Surg. 2010;200(1):47–52.
118. Armstrong PA, Back MR, Bandyk DF, Johnson BL, Shames ML.Selective application of sartorius muscle aps and aggressive staged surgical debridement can inuence long-term outcomes of complex prosthetic graft infections. J Vasc Surg. 2007;46(1):71–8.
119. Siracuse JJ, Nandivada P, Giles KA, Hamdan AD, Wyers MC, Chaikof EL, etal. Prosthetic graft infections involving the femoral artery. J Vasc Surg. 2013;57(3):700–5.
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120. Lyons OT, Patel AS, Saha P, Clough RE, Price N, Taylor PR.A 14-year experience with aortic endograft infection: management and results. Eur J Vasc Endovasc Surg. 2013;46(3):306–13.
121. Smeds MR, Duncan AA, Harlander-Locke MP, Lawrence PF, Lyden S, Fatima J, etal. Treatment and outcomes of aortic endo­graft infection. J Vasc Surg. 2016;63(2):332–40.
122. Lawrence PF. Conservative treatment of aortic graft infection. Semin Vasc Surg. 2011;24(4):199–204.
123. Belair M, Soulez G, Oliva VL, Laperriere J, Gianfelice D, Blair JF, etal. Aortic graft infection: the value of percutaneous drainage. AJR Am J Roentgenol. 1998;171(1):119–24.
124. Morris GE, Friend PJ, Vassallo DJ, Farrington M, Leapman S, Quick CR. Antibiotic irrigation and conservative surgery for major aortic graft infection. J Vasc Surg. 1994;20(1):88–95.
125. Samoukovic G, Bernier PL, Lachapelle K.Successful treatment of infected ascending aortic prosthesis by omental wrapping without graft removal. Ann Thorac Surg. 2008;86(1):287–9.
126. Antoniou GA, Koutsias S, Antoniou SA, Georgiakakis A, Lazarides MK, Giannoukas AD. Outcome after endovascular stent graft repair of aortoenteric stula: a systematic review. J Vasc Surg. 2009;49(3):782–9.
127. Xiromeritis K, Dalainas I, Stamatakos M, Filis K.Aortoenteric stulae: present-day management. Int Surg. 2011;96(3):266–73.
128. Alonso M, Caeiro S, Cachaldora J, Segura R.Infected abdominal aortic aneurysm: in situ replacement with cryopreserved arterial homograft. J Cardiovasc Surg (Torino). 1997;38(4):371–5.
129. Bandyk DF, Novotney ML, Back MR, Johnson BL, Schmacht DC. Expanded application of in situ replacement for prosthetic graft infection. J Vasc Surg. 2001;34(3):411–9. discussion 9-20.
130. Vardanian AJ, Chau A, Quinones-Baldrich W, Lawrence PE. Arterial allograft allows in-line reconstruction of prosthetic graft infection with low recurrence rate and mortality. Am Surg. 2009;75(10):1000–3.
131. Lehnert T, Gruber HP, Maeder N, Allenberg JR.Management of primary aortic graft infection by extra-anatomic bypass recon­struction. Eur J Vasc Surg. 1993;7(3):301–7.
132. Ali AT, Modrall JG, Hocking J, Valentine RJ, Spencer H, Eidt JF, etal. Long-term results of the treatment of aortic graft infection by in situ replacement with femoral popliteal vein grafts. J Vasc Surg. 2009;50(1):30–9.
133. Clagett GP, Valentine RJ, Hagino RT. Autogenous aortoiliac/ femoral reconstruction from supercial femoral-popliteal veins:
feasibility and durability. J Vasc Surg. 1997;25(2):255–66. discus­sion 67-70.
134. Yeager RA, Moneta GL, Taylor LM Jr, Harris EJ Jr, McConnell DB, Porter JM.Improving survival and limb salvage in patients with aortic graft infection. Am J Surg. 1990;159(5):466–9.
135. Yeager RA, Taylor LM Jr, Moneta GL, Edwards JM, Nicoloff AD, McConnell DB, et al. Improved results with conventional man­agement of infrarenal aortic infection. J Vasc Surg. 1999;30(1): 76–83.
136. Bunt TJ.Synthetic vascular graft infections. I.Graft infections. Surgery. 1983;93(6):733–46.
137. Yashar JJ, Weyman AK, Burnard RJ, Yashar J.Survival and limb salvage in patients with infected arterial prostheses. Am J Surg. 1978;135(4):499–504.
138. Ricotta JJ, Faggioli GL, Stella A, Curl GR, Peer R, Upson J, etal. Total excision and extra-anatomic bypass for aortic graft infec­tion. Am J Surg. 1991;162(2):145–9.
139. Sharp WJ, Hoballah JJ, Mohan CR, Kresowik TF, Martinasevic M, Chalmers RT, et al. The management of the infected aor­tic prosthesis: a current decade of experience. J Vasc Surg. 1994;19(5):844–50.
140. Noel AA, Gloviczki P, Cherry KJ Jr, Sa H, Goldstone J, Morasch MD, et al. Abdominal aortic reconstruction in infected elds: early results of the United States cryopreserved aortic allograft registry. J Vasc Surg. 2002;35(5):847–52.
141. Oderich GS, Bower TC, Cherry KJ Jr, Panneton JM, Sullivan TM, Noel AA, etal. Evolution from axillofemoral to in situ prosthetic reconstruction for the treatment of aortic graft infections at a sin­gle center. J Vasc Surg. 2006;43(6):1166–74.
142. Zhou W, Lin PH, Bush RL, Terramani TT, Matsuura JH, Cox M, etal. In situ reconstruction with cryopreserved arterial allografts for management of mycotic aneurysms or aortic prosthetic graft infections: a multi-institutional experience. Tex Heart Inst J. 2006;33(1):14–8.
143. Koskas F, Goeau-Brissonniere O, Nicolas MH, Bacourt F, Kieffer E. Arteries from human beings are less infectible by Staphylococcus aureus than polytetrauoroethylene in an aortic dog model. J Vasc Surg. 1996;23(3):472–6.
144. Berger P, Van Herwaarden JA, Harkisoen S, De Vries JP, Ekkelenkamp M, Moll FL.Surgical treatment of infected aortic grafts. J Cardiovasc Surg. 2012;53(6):719–34.
Surgical Treatment
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oftheThoracic Aorta
JuanJoseGallegos Jr., GeorgeArnaoutakis, DeanJ.Arnaoutakis, KirstenA.Freeman, DavidJereyHall, andMahmoudAlhussaini
18
Perfusion Techniques forProximal Aortic Aneurysms
Cardiopulmonary bypass (CPB) (Fig. 18.1) is utilized for providing circulatory support in ascending aortic aneurysms (aortic annulus to innominate artery). If the involvement is restricted to the aortic root or ascending aorta alone, then CPB is sufcient. When aneurysmal disease involves the arch, or arch repair is anticipated, circulatory arrest is gener­ally required. There are multiple approaches to circulatory arrest including deep hypothermia without cerebral perfusion and varying degrees of hypothermia with cerebral perfusion. The best strategy for cerebral protection is currently under debate and is a focus of active investigation. Options include deep hypothermia (18–22 °C), moderate hypothermia (22– 26°C), and mild hypothermia (26–30 °C). Cannulation for arch disease depends on the cerebral perfusion strategy. Direct aortic cannulation with dual-stage right atrial cannula can be used in selective antegrade cerebral circulation via direct arch vessel ostia once circulatory arrest is initiated (Fig.18.2). Multiple techniques are available in clinical prac­tice for cerebral perfusion: (1) retrograde cerebral perfusion, (2) selective unilateral antegrade cerebral perfusion via right axillary perfusion, and (3) direct bilateral antegrade cerebral perfusion via ostia of the arch vessels (Fig.18.2). When com­paring antegrade versus retrograde cerebral perfusions during deep hypothermic circulatory arrest, there is no difference in 30-day mortality or stroke in the postoperative period [1]. When comparing deep hypothermic circulatory arrest to moderate hypothermic arrest, there are shorter cross clamp
times, shorter cardiopulmonary bypass times, and fewer transfusion requirements during moderate hypothermic circu­latory arrest [2]. Some studies have shown moderate hypo­thermic arrest is also associated with fewer neurologic sequelae compared to deep hypothermic arrest and lower 30-day mortality; however, no randomized data exist [3].
Surgical Technique
The patient is positioned supine and a roll is placed between the scapulae to allow greater exposure to the sternum and medias­tinum. The neck should be extended which is particularly help­ful for patients with large body habitus. The arms are tucked to the side. Body hair is clipped, and the patient is prepped from the angle of the mandible to feet. Care is taken to stay midline while performing the sternotomy. The sternal periosteal vessels are coagulated, and vancomycin paste is applied to the sternal edges. Although the utility of vancomycin applied to sternal edges is highly debated, several studies have found signicant reduction in supercial and deep wound infections [47]. A sternal retractor is used to expose the anterior mediastinum. The thymus is separated midline up to the innominate vein. The pericardium is opened from the diaphragmatic pericardium up to the superior pericardial reection and transversely at the superior and inferior portion of the pericardium. If the arch is uninvolved, there is minimal dissection needed onto the arch of the aorta. Circumferential dissection of the aorta is carried out in preparation for replacement with graft.
J. J. Gallegos Jr. (*) · K. A. Freeman · D. J. Hall · M. Alhussaini G. Arnaoutakis Department of Surgery, Division of Thoracic and Cardiovascular Surgery, University of Florida, Gainesville, FL, USA
D. J. Arnaoutakis Department of Surgery, Division of Vascular and Endovascular Surgery, University of Florida, Gainesville, FL, USA
© Springer Nature Switzerland AG 2019 R. S. Dieter et al. (eds.), Diseases of the Aorta, https://doi.org/10.1007/978-3-030-11322-3_18
Repair ofAortic Root andAscending Aortic Aneurysms
Root repair can be performed in many fashions, with com­posite replacements being more common compared to valve­sparing procedure. Composite mechanical prosthesis is generally chosen for younger patients with few comorbidities.
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Cardiopulmonary bypass Left heart bypass
Ar
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SVC
IVC
terial
outflow
RA
RV
LA
Aorta
Pump sucker
SVC
LV vent
LV
Reservior
Pump
RA
RV
IVC
Aorta
LA
LV
Oxygenator Heart
Fig. 18.1 Partial cardiopulmonary bypass versus left heart bypass for open TAAA repair
Biologic composites are often reserved for those in advanced age who could not tolerate anticoagulation. Bioprosthetic valves additionally offer patients many benets such as free­dom from anticoagulation and potential for transcatheter replacement if structural degeneration occurs.
All patients undergo intraoperative transesophageal echo­cardiography (TEE) to evaluate for aortic valve insufciency or other aortic pathology which may alter the therapeutic approach. For ascending aorta replacement alone, cannulation of the aorta should be distal enough to allow cross clamp and anastomosis to healthy aorta. If the diseased segment extends to the level of the innominate artery, this may require circula­tory arrest to achieve adequate aortic replacement. If circula­tory arrest is contemplated because the aneurysm approaches zone 1 of the aorta, then the cannulation site need not be distal on the aortic arch. The atrium is then cannulated with a dual­stage cannula. A ventricular vent catheter is strongly recom­mended in all aortic root procedures, as manipulation of the aorta may cause aortic insufciency. When the integrity of the proximal arch is in question, hypothermic circulatory arrest is used to allow for complete inspection of the arch.
Prior to cannulation, the patient is given heparin (400units/kg), and cardiopulmonary bypass is instituted at
an activation clotting time (ACT) of greater than 480s. The patient is cooled to 22–28°C.While cooling, any further dis­section is completed prior to cross clamping. The cross clamp is applied, and cardioplegia is administered. A trans­verse aortotomy is performed at the sinotubular junction. The distal segment of aorta the ascending aorta is then removed. For aortic root replacement, the right and left coro­nary buttons are fashioned by sharp excision leaving enough aorta around the ostia to allow for a safe anastomosis to the graft/tissue. The aortic root is completely mobilized using a combination of sharp and cautery dissection.
The aortic root anastomosis is completed with composite conduit with 2–0 polyester suture pledgeted horizontal mattress sutures. The suture line is dried and Bioglue may be applied to the suture line particularly in friable tissues. The right and left coronary buttons are sized and location on the conduit chosen for the anastomoses. It is imperative to have sufcient mobility on both coronary buttons to ensure a tension- free anastomosis. The ostial sites are then opened with a high-temperature cautery pen. If a biologic conduit is being used such as homograft or xenograft root, a 4mm punch is used to create the ostial sites. The left coronary button is rst anastomosed followed by the right coronary button.
Pump
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Fig. 18.2 Selective antegrade cerebral perfusion vial ostia of arch
vessels
The distal anastomosis is performed proximal to the aor­tic clamp with a 4-0 polypropylene suture in a running fash­ion. If the aorta is thin or of poor quality, then a felt strip is used to bolster the anastomosis. Bioglue can be applied to the distal anastomosis, and the aorta is deaired prior to removing the cross clamp (Fig.18.3).
Ascending Aortic Aneurysms
Supravalvular aortic aneurysms are treated with tube graft replacement of the ascending aorta. Aortic arch or innominate artery cannulation is performed, which allows for innocuous manipulation of the proximal aorta during anastomosis. Venous cannulation is performed with a dual-stage cannula. Prior to initiating cardiopulmonary bypass, the ascending aorta is evaluated for the cross-clamp site. For isolated tube graft replacement of the ascending aorta, mild hypothermia is used unless prolonged bypass is anticipated, as in cases where concomitant cardiac procedures are performed.
Once cardiopulmonary bypass is initiated, the ascending aorta is resected distal to the sinotubular junction to distal disease-free margin of the distal ascending aorta. 4-0 poly­propylene suture is used to create a running anastomosis.
279
Bioglue can be administered to the aortic anastomosis (Fig.18.4). If the proximal aortic arch is involved, moderate hypothermia is utilized, and a brief period of circulatory arrest is used with selective antegrade cerebral perfusion.
Aortic Arch Disease
Aortic arch disease involves a unique set of challenges. When considering treatment options for patients with arch disease, one must take into consideration the extent of the disease and assess the need for descending aorta repair. These issues will direct the optimal cannulation strategy. Preferentially, right axillary ante­grade ow which allows selective unilateral antegrade cerebral perfusion or direct aortic cannulation with ostial cerebral perfu­sion while on circulatory arrest is chosen over retrograde cere­bral perfusion or no cerebral perfusion. In the context of a patient with cerebral vascular disease or circle of Willis that is not in continuity or diseased, direct cannulation and perfusion of the arch vessels is a better alternative once on circulatory arrest. Venous cannulation is performed with dual-stage cannula. Options for arch replacement are tube graft to the distal aortic arch with an end-to-side anastomosis of the arch island as a patch. A triple-branch arch graft with a side arm to re- establish perfusion through the graft once the distal and arch vessel anas­tomosis are complete is the preferred graft choice because it avoids the risk of subsequent patch aneurysm formation.
Once cardiopulmonary bypass is initiated, the patient is cooled to 22°C.The extent of the aortic aneurysmal disease is inspected. Antegrade cardioplegia is administered, and then diseased aorta is resected. The innominate artery is clamped proximal to the right axillary artery and carotid bifurcation. Selective antegrade ow is set at 10cc/kg/min of ow, and distal perfusion is ceased. To ensure antegrade perfusion is functioning, we visualize ow through the left common carotid and left subclavian arteries. Bilateral cerebral oxime­try and electroencephalography are important monitoring adjuncts to ensure adequate cerebral protection. If there are concerns during unilateral antegrade cerebral perfusion, direct ostial cannulation of the left carotid is implemented for cerebral protection. Another alternative is retrograde cerebral perfusion, but this modality is preferred for shorter circula­tory arrest times such as hemiarch replacement only.
The anastomoses are started distal to proximal. The rst anastomosis is to the descending aorta. This is completed in a similar fashion as the distal ascending arch repair, gener­ally using a 3–0 polypropylene and felt strip, with Bioglue around the anastomosis. The subclavian artery anastomosis is typically performed under circulatory arrest to assist with visualization, using a 4–0 polypropylene suture (Fig.18.5). The side branch of the graft can be recannulated and cardio­pulmonary bypass re-established to achieve distal organ per­fusion. The left carotid and innominate artery anastomoses are then sequentially performed, taking care to de-air each of
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Fig. 18.3 (a–d). The
complete Bentall procedure
J. J. Gallegos Jr. et al.
a
b
c
these anastomoses prior to re-establishing antegrade ow. The proximal anastomosis is performed in the same manner as above. De-airing maneuvers are performed, and the clamp is released while the patient is rewarmed.
d
tion [10]. The risk of mortality increases with renal injury up to 10% depending on the degree of renal dysfunction [9]. Hospital volume contributes to surgical outcomes in proximal aortic dis­ease as well. Centers with high volume have a mortality rate of 1–3.4% compared to 5.8% in low- volume centers [9, 11].
Outcomes andComplications
Mortality
Survival from proximal aorta and arch aneurysms is variable. Elective replacement of the proximal aorta carries a mortality rate of 1–3.4%, whereas it is up to 15.4% for nonelective cases [8, 9]. There are many factors that contribute to mortality including urgency of the case, age, ventricular function, arch surgery, concomitant coronary surgery, pulmonary disease, nonsinus rhythm, female sex, NYHA >II, and renal dysfunc-
Complications
Elective proximal aortic surgery can be accomplished rela­tively safely with good outcomes. However, the commonly encountered complications include cerebrovascular acci­dent, temporary neurologic dysfunction, hemorrhage, and pulmonary and renal dysfunction. The occurrence of a com­plication contributes not only to length of stay but mortality.
Coagulopathy is caused by many interacting factors: hypo­thermia, inammation, and anticoagulation. Preoperative
Graft
ta
ab c
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disseminated intravascular coagulation has been described in aortic aneurysms [12]. Ultimately, abnormalities in the clot­ting cascade lead to increased transfusions. Cardiopulmonary bypass induces a proinammatory state. Its utilization, par­ticularly with prolonged bypass times, can lead to end-organ damage along with coagulopathy. Visceral injury from car­diopulmonary bypass can be caused by hypoperfusion [13].
Aor
It is difcult to quantify these conditions as surgical approach, length of surgery, length of cardiopulmonary bypass, length of circulatory arrest, and volume of surgical interventions vary from surgeon to surgeon.
Stroke is a complication of aortic surgery and varies depending on urgency of the intervention. The majority of strokes are embolic [14]. The length of cerebral ischemia is correlated to increased rates of stroke. There have been decreased rates of stroke with the combination of hypother­mia, cannulation strategies, and antegrade cerebral perfusion.
Long-Term Survival
As surgical techniques continue to evolve, long-term survival has improved. Long-term mortality decreased from 16.7% to
11.6% from 1992 to 2004 at 60days and varies between 32% and 57% at 10years when evaluating dissections and aneu­rysms [1517]. Most commonly, mortality is associated with cardiac or aortic correlating to the age of the patient [15, 18]. Age greater than 60 is independently associated with long­term mortality [18]. Five percent of patients at 5years will have reoperations and at 10years nearly 8% [18].
Fig. 18.4 Completed ascending aortic aneurysm repair
Fig. 18.5 (a–c) Completion
of aortic arch repair
SCP
Surgical Treatment ofDescending Thoracic andThoracoabdominal Aneurysms
Introduction
While open repair of descending thoracic aortic aneurysms (TAAs) and thoracoabdominal aortic aneurysms (TAAAs) remains the gold standard for the treatment of these complex disease processes, it involves some of the most challenging preoperative planning, intraoperative decision making, and postoperative care that surgeons encounter. Successful
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outcomes not only require appropriate patient selection and meticulous execution of chosen repair but have also evolved to include adjuncts for end-organ and spinal cord protection and protocol-driven postoperative care to limit morbidity related to spinal cord ischemia (SCI) and renal failure.
Intraoperative Considerations
Anesthesia
The usual setup for DTAA or TAAA repairs includes a double- lumen endotracheal tube, central lines, a pulmonary artery catheter (for hemodynamic monitoring), a transesoph­ageal echocardiogram (TEE) probe (to optimize cardiac function and to guide cannula placement if using CPB), and arterial lines (in both the upper and lower extremities to monitor both proximal and distal perfusion during aortic clamping). Lumbar cerebrospinal uid (CSF) drains are used routinely for Crawford extent I and II repairs [19]. The target CSF pressure is typically 7–10mm Hg with drainage over the chosen pressure. Cranial and peripheral electrodes are placed for monitoring of somatosensory or motor evoked potentials to assess intraoperative spinal cord protection and perfusion [20]. Mannitol and sodium bicarbonate infusion are commonly administered to protect the kidneys while the aorta is occluded [21]. Blood counts are checked frequently throughout the operation and cell saver, packed red blood cells, and fresh frozen plasma are transfused as necessary. If vasodilators are needed, nitroprusside and hydralazine should be avoided due to their potential detrimental effects on ischemic tolerance of the spinal cord [22].
Perfusion Techniques
Regarding circulatory support for TAAA repair, most groups advocate either left heart bypass (LHB) or partial cardiopul­monary bypass (Fig.18.1) [19, 23]. With LHB, oxygenated blood from the heart is delivered to a centrifugal pump via a cannula inserted into the left atrium or the left inferior pul­monary vein. The pump then delivers the blood to the distal aorta including its visceral and pelvic branches through a cannula that is inserted directly into the femoral or iliac artery, or into an 8mm Dacron conduit that has been sewn to the left common femoral artery. This technique is benecial as it reduces cardiac strain despite the proximal aortic clamp­ing and decreases the incidence of ischemia-associated com­plications such as metabolic acidosis, acute renal failure, and paraplegia. Also, it avoids the inammatory insult associated with the use of a membrane oxygenator [24].
Alternatively, some groups prefer partial cardiopulmo­nary bypass achieved through femoral arterial cannulation (either direct cannulation or through an 8mm Dacron graft) and bicaval venous cannula inserted through the left femoral vein and positioned in the center of the right atrium under
TEE guidance to allow for blood return to the oxygenator. By monitoring radial and femoral arterial lines, the blood pressure proximal and distal to the aortic cross-clamps can be manipulated by adjusting the pump ow and venous drainage. This technique reduces strain on the right side of the heart despite the proximal aortic clamping and is bene­cial in patients with poor pulmonary function who may not tolerate single lung ventilation [
25, 26]. In cases where a
proximal clamp site is not feasible, circulatory arrest is man­datory for construction of the proximal anastomosis [27]. The same cannulation strategy can be used but in conjunc­tion with deep hypothermic circulatory arrest (DHCA) and subsequent total body retrograde perfusion, enabling a uni­form strategy for all TAAA repairs [28].
Spinal Cord Protection
Numerous strategies have been implemented to reduce the risk of spinal cord ischemia associated with TAA and TAAA repair.
Spinal Cord Protection Strategy During Descending and Thoracoabdominal Aortic Aneurysm Repair
Anatomical
• Motor evoked potential monitoring to identify criti­cal segmental arteries to reattach
• Sequential aortic clamping when possible
Physiological
• Moderate heparinization (1mg/kg)
• Permissive mild hypothermia (32–34 °C, nasopharyngeal)
• Cerebrospinal uid drainage
• Left heart bypass during proximal anastomosis
Naturally, the risk of spinal cord injury (SCI) increases when fewer radicular arteries are patent after TAAA, which varies by the underlying aortic pathology as well as the extent of aortic replacement. This concept led surgeons to selectively or nonselectively reimplant intercostal arteries [29, 30], but this strategy seems to have limited benet in those with aneurysmal disease and an almost negligible role in those with acute dissection [31, 32]. Jacobs and colleagues elegantly demonstrated that intraoperative neurologic moni­toring with motor evoked potentials (MEPs) can be used to help identify critical intercostal arteries for revascularization and augment hemodynamics in order to reverse SCI [20]. A sudden drop in MEP amplitude following sequential clamp­ing prompts an increase in distal perfusion pressures; if MEPs do not rebound, then intercostal vessels in the involved
18 Surgical Treatment oftheThoracic Aorta
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segment are reimplanted with an inclusion button. Patients with extensive Type II TAAAs derive the most benet from the use of MEPs with targeted intercostal reimplantation as opposed to those with less extensive TAAAs [32].
Additionally, there are several physiologic maneuvers that have been shown to diminish the risk of SCI.These include hypothermia, decreasing spinal pressure via CSF drainage, increasing mean arterial pressure (MAP), main­taining oxygen delivery to tissues by avoiding anemia and hypoxia, and neurochemical protection with naloxone, ste­roids, and burst suppression [33, 34]. In fact, sophisticated work by Acher and colleagues has shown that these physi­ologic parameters account for 80% of paraplegia risk, whereas intercostal blood ow is responsible for 20% of risk [32].
Moderate hypothermia (32°C) has been shown in animal models to confer SCI protection for up to 50min [35]. Some studies suggest that DHCA (15–20°C) may offer even greater spinal cord protection with TAAA repair [36]. The systemic temperature goal is typically achieved actively with the use of a heat exchanger within a CPB circuit. Using CPB allows for active rewarming of the patient but with risk of coagulo­pathic bleeding, pulmonary dysfunction, and cardiac arrhyth­mias, all of which are more profound if deep hypothermia is utilized [27]. In contrast to active cooling, passive systemic cooling can be accomplished through the administration of cold intravenous uids and avoidance of external warming mechanisms. An alternative option is regional hypothermia whereby an epidural infusion system is used to instill iced saline into the watershed zone of the spinal cord, taking care to avoid increasing CSF pressure [37].
CSF drainage effectively acts to increase spinal perfusion pressure by decreasing CSF pressure to 8mm Hg intraopera­tively and 10mm Hg postoperatively. Two randomized trials from the same center have shown conicting results with CSF drainage [38, 39]. Nonetheless, most agree that CSF drainage remains central to a spinal cord protection protocol.
Additional physiologic adjuncts can include the adminis­tration of steroids methylprednisolone (30mg/kg) and man­nitol (12.5 g) during anesthesia induction to reduce ischemia-reperfusion injury. Mannitol not only decreases CSF pressure and preserves urine ow after renal ischemia but also acts as a free radical scavenger [21]. Acher and col­leagues also utilize a naloxone infusion (1 mcg/kg/hr) because it has been shown to decrease excitatory neurotrans­mitters from ischemic neurons [40]. Finally, MAP is typi­cally maintained above 100 mm Hg while the aorta is clamped, and hemoglobin concentrations should be kept 10g/dL to help preserve spinal cord oxygen delivery. The importance of maintaining goal arterial pressure cannot be overemphasized, as most causes of delayed SCI likely arise from brief periods of postoperative hypotension [41].
Visceral Organ Protection
Some of the methods used for spinal cord protection addi­tionally aid in preventing ischemic injury of the abdominal viscera. These include permissive hypothermia and sequen­tial aortic clamping in the repair of any TAAA.Additionally, cold crystalloid selective renal perfusion and selective perfu­sion of the celiac and superior mesenteric axes are frequently employed in extent I and II TAAA repairs [42]. This is accomplished utilizing balloon-tipped catheters and a sepa­rate arterial inow circuit from the bypass pump to perfuse the celiac and superior mesenteric vascular beds with oxy­genated blood, particularly during the reattachment of proxi­mal thoracic aortic segmental arteries.
Surgical Approach
Surgical Positioning andExposure
The patient is placed in a modied right lateral decubitus position with padding of all pressure points and a right axil­lary roll to protect the axillary nerve (Fig.18.6). The hips are rotated obliquely to the left to allow access to the right groin, if necessary. The right knee is exed, and the left kept straight, with padding between the legs to avoid stretch on the left femoral nerve. A beanbag is used to maintain this position and the table is exed just above the iliac crest. The eld is prepped to include the left chest including the axilla superiorly and the spine posteriorly. The entire abdomen and both groins are prepped.
An incision along the fth or sixth intercostal space is adequate for most Type I and Type II TAAAs. Type III TAAAs are approached through the seventh or eighth inter­costal space and Type IV TAAAs through the ninth inter­space. The incision is extended down along the abdominal wall onto the left lower quadrant, staying lateral to the left rectus muscle. The costal margin is divided connecting the retroperitoneum to the chest cavity. The retroperitoneal plane is developed deep to the transversus abdominus muscle tak­ing care to not violate the peritoneum, which can be quite thin medially. Care should be taken upon entering the abdo­men to clearly identify the external and internal oblique lay­ers, as their identication aids in closure later in the case. After the costal margin is divided, the diaphragm is incised circumferentially taking care to avoid injury to the phrenic nerve but leaving enough diaphragmatic cuff on the chest wall to facilitate closure. The left kidney and viscera are reected medially, exposing the aorta from the hiatus to the iliac bifurcation. At this point, single-lung ventilation can be used, and a self-retaining retractor system should be placed to maintain exposure.
The left inferior pulmonary ligament is divided, and the lung is mobilized from the aneurysm. The extent of proximal exposure again depends on the location of aortic disease.
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60˚
Hips
30˚
Fig. 18.6 Patient positioning. For repair of the descending thoracic aorta, the patient is positioned in modied right lateral decubitus position. The
surgical incision extends from the left scapula through the fth to seventh intercostal space across the costal margin and toward the left periumbili­cal region to allow the surgeon to enter the retroperitoneal space
Care should be taken to identify and avoid injury to the phrenic, vagus, and recurrent laryngeal nerves, which are encountered during the dissection of the proximal thoracic aorta. If repairing a TAAA, the abdominal aortic branches are now exposed dissecting free the celiac artery (CA), supe­rior mesenteric artery (SMA), and left renal artery (LRA). Sufcient exposure of the SMA and CA to allow clamp placement will prevent unnecessary blood loss from back bleeding upon opening the aneurysm sac.
Repair oftheDescending Thoracic Aorta Segment
After sufcient exposure, the sequence and method of aortic reconstruction can proceed in a variety of ways depending on surgeon preference. The basic principles are to facilitate the completion of the reconstruction, prevent spinal cord injury, and allow perfusion of the branch vessels/lower extremities for as long as possible through each step to avoid ischemia/ reperfusion injury of the end organs.