Добавил:
kiopkiopkiop18@yandex.ru t.me/Prokururor I Вовсе не секретарь, но почту проверяю Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз: Предмет: Файл:

Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3734_Библиотеки_им_академика_М_И_Перельмана

.pdf
Скачиваний:
0
Добавлен:
31.08.2026
Размер:
27 Мб
Скачать
356
https://t.me/med1917
E. Iannacone et al.
occurs from the dissecting ap or false lumen obstructing the ostia of the great ves­sels (Fig.4) [28].
Some consider cerebral malperfusion itself to be a contraindication to immediate repair. The prominent concerns with immediate central repair, most often done with concurrent hypothermic circulatory arrest and with full anticoagulation, include the risk of hemorrhagic conversion and reperfusion injury worsening neurologic out­come. Patients with ATAAD and cerebral malperfusion are also more likely to pres­ent with other characteristics predictive of poor outcomes, including hypotension, shock, tamponade, renal failure, myocardial ischemia, and limb ischemia. The risk of delaying surgery for stabilization of the neurologic condition, however, includes rupture and death. According to recent IRAD data, surgery is signicantly less likely to be performed in patients with coma (66.7%) or stroke (75.9%) than those without a brain injury (88.9%). However, patients with ATAAD and brain injury perform miserably when managed medically, with a 100% mortality if presenting with coma. Only 12.8% of those with CVA managed medically survive to discharge. Although CVA and coma predict at least a two- or threefold higher mortality, patients who receive surgical treatment have a 75% survival to discharge [29].
There are some reports of novel techniques for early cerebral reperfusion includ­ing direct carotid perfusion, endovascular stenting, or direct surgical fenestration, followed by central repair [3032]. Our standard approach is immediate central repair of the dissection. Central cannulation of the true lumen is our preferred arte­rial cannulation strategy. We utilize a Seldinger technique and the guidance of both epiaortic ultrasound and transesophageal echocardiography to ensure true lumen perfusion [33]. Near-infrared spectroscopy (NIRS) conrms symmetric great vessel ow, thus eliminating the need to manipulate the great vessels. In the small number of patients in which we are unable to access the true lumen centrally, we utilize the femoral artery for arterial inow and only use axillary artery cannulation as a last resort. In our experience, the depth of the axillary artery, fragility of the vessel, and the need to place a perfusion graft onto the artery a majority of the time leads to additional cerebral ischemic time that can be avoided.
Fig. 4 Acute type A aortic dissection with innominate artery dissection and occlusion of right carotid artery (arrow)
Management of Complicated Type A Aortic Dissection: The Cornell-New York…
https://t.me/med1917
Intraoperative cerebral monitoring can include any combination of electroen­cephalogram, NIRS, and transcranial Doppler ultrasound. We routinely use NIRS (Somanetics INVOS Cerebral/Somatic Oximeter, Covidien, IL, USA) to evaluate cerebral perfusion, particularly during the initiation of cardiopulmonary bypass or with aortic cross clamping. A sharp decrease in the cerebral oxygenation suggests the need for alternative arterial cannulation or removal of the cross clamp for the remainder of cooling. Although the optimal cerebral protection strategy during arch surgery is often debated, a recent network meta-analysis of 26,968 patients, in which dissections were included, compared deep hypothermic circulatory arrest with antegrade (ACP) and retrograde cerebral perfusion (RCP). The authors found no difference between ACP and RCP for stroke or operative mortality [34]. We prefer RCP and deep hypothermic circulatory arrest (DHCA) with a systemic tem­perature of 20°C or less. In the setting of cerebral perfusion we prefer a conserva­tive strategy of hemiarch reconstruction to limit cerebral ischemic time and quickly reestablish antegrade great vessel ow.
Patient selection has been crucial to improving surgical outcomes over the last two decades. Although quality of life data is not readily available for patients sur­viving immediate surgical management of ATAAD with cerebral malperfusion, sev­eral studies have reported favorable outcomes [28, 29, 32, 35]. Complete resolution of neurologic decits have been reported in up to 84% of patients presenting with focal decits. Patients with more devastating neurologic injury are signicantly less likely to achieve neurologic improvement. Neither cerebral protection method nor extent of aortic arch repair appear to be predictive of neurologic improvement. Early intervention, however, particularly within 10h of presentation of stroke, is integral to achieving neurologic recovery [28, 35]. This data should encourage surgeons to offer emergent surgery to selected patients, particularly those with focal decits, despite their higher risk prole.
357
Spinal Malperfusion
Spinal malperfusion complicating ATAAD is rare, occurring in less than 5% of patients [4, 18]. It manifests as paraparesis or paraplegia, may present unilaterally, and may be accompanied by urinary or bowel incontinence. Immediate central aor­tic repair is the mainstay of treatment, with complete resolution of spinal cord injury occurring in 61% [18]. The presence of preoperative spinal malperfusion is associ­ated with increased risk of postoperative complications, and signicantly increased risk of mortality [4]. Resolution of spinal ischemia, however, is protective against the increased risk of early mortality seen by those who do not experience neurologic recovery [18]. The presence of preoperative spinal malperfusion should not deter surgeons from offering a potentially life-saving procedure. Although nearly 40% of patients do not experience complete resolution of their symptoms, there may be an opportunity for those with partial recovery to experience additional return of lower extremity function with extensive rehabilitation.
358
https://t.me/med1917
E. Iannacone et al.
Mesenteric Malperfusion
Mesenteric malperfusion is fortunately a rare complication of ATAAD, occurring in 4–6% of patients [4, 36]. It can be insidious in presentation and frequently presents with malperfusion of other vascular territories. Patients with mesenteric MPS may present with abdominal pain, melena, metabolic acidosis, or elevated liver enzymes. The etiology may be dynamic obstruction, occlusive, or thromboembolic. The pres­ence of mesenteric MPS is highly lethal, with nearly two-thirds of patients dying during hospitalization, a threefold increase over those without the complication [4, 36].
Management strategies for mesenteric malperfusion are perhaps the most strongly debated. The traditional approach of immediate aortic repair remains the most commonly utilized. Despite this, nearly one third of patients diagnosed with mesenteric ischemia are treated “medically” according to recent IRAD data. This likely reects surgeons’ acknowledgement that, even with repair, mesenteric malp­erfusion is one of the most threatening dissection-related complications. Without intervention, however, less than 5% survive [36].
Over recent decades, some groups have dedicated their efforts to a peripheral revascularization rst strategy in order to resolve the MPS before moving on to primary aortic repair [3741]. This approach relies heavily on early identication of patients who are at great risk of death from end-organ failure, and the availability of proceduralists and facilities skilled at performing complex interventional proce­dures. The theoretical benet to this approach is that resolving the MPS will reduce systemic inammation and metabolic derangements that otherwise would increase the risk of central repair [16]. It may also prevent a futile attempt at open aortic repair for the already unsalvageable patient who succumbs to organ failure despite reperfusion of the affected vascular bed. Avoiding preventable aortic rupture while awaiting resolution of MPS is the biggest challenge of the staged approach. Yang and colleagues were able to eliminate fatal aortic rupture with their modied algo­rithm (Fig.5), noting that they enforced strict hemodynamic management during the endovascular phase and waited only for downtrending rather than normalization of ischemic markers before central repair. Despite this, total mortality for patients with mesenteric MPS remained high, 33.3–40.3% [38]. Those presenting with stroke (odds ratio [OR] 23), lactate >6mmol/L (OR 13.5), or with bowel necrosis at laparotomy (OR 7) are the most difcult to salvage [37].
In many practices, including ours, the most expeditious means to restore end­organ function is rapid transfer to the operating room. We most often establish ante­grade ow into the true lumen early by central cannulation, followed by rapid conservative aortic repair. The risk of rupture or fatal tamponade complicating delayed central repair is eliminated, and metabolic derangements can be corrected while on bypass. Persistently elevated lactates in the operating room after central aortic repair or high risk preoperative prole may warrant immediate laparotomy after central repair. Ongoing postoperative clinical or biochemical evidence of
No
Management of Complicated Type A Aortic Dissection: The Cornell-New York…
https://t.me/med1917
Acute type A aortic dissection
359
Hemodynamic instability
(aortic rupture, tamponade)?
No
Visceral or extremity
malperfusion syndrome (MPS)?
Ye s
Arterial obstruction?
Ye s
Endovascular treament
(fenestration/stenting)
Optimal medical support in ICU
Hemodynamic instability
(aortic rupture, tamponade)?
No
Resolution of organ failure?
Ye s
No
No
Open aortic repair
Ye s
Ye s
Fig. 5 Michigan algorithm for acute type A aortic dissection and mesenteric or extremity malper­fusion syndrome (MPS). ICU indicates intensive care unit [38]
persistent bowel ischemia after central repair should prompt mesenteric angiogra­phy with interventional fenestration, angioplasty, or stenting, accompanied by abdominal exploration and resection of any ischemic bowel. Patients presenting with the particularly moribund risk factors of concomitant stroke or severely ele­vated lactate may be considered for a staged approach.
Mortality rates for patients with ATAAD complicated by mesenteric MPS are dismal with medical and endovascular therapies alone [36]. Disappointingly, how­ever, when comparing the endovascular rst to central repair rst approaches, the overall mortality for patients with mesenteric MPS complicating ATAAD is still alarmingly high [42]. Ongoing efforts supporting more prompt detection and resto­ration of mesenteric blood ow is paramount to improving outcomes for this extremely high-risk cohort.
360
https://t.me/med1917
E. Iannacone et al.
Peripheral Malperfusion
Peripheral malperfusion complicates ATTAD in 10–13% of patients in larger regis­tries, and often accompanies malperfusion of other vascular beds [1, 3, 4, 17, 43]. Limb ischemia manifests early as a cool, pulseless extremity with mottled skin, later as sensory and motor decits and, in its most advanced stage, as profound paralysis of the limb [44]. Signicant preoperative elevations in creatine kinase may signal potentially irretrievable tissue damage [45]. Sequelae of limb reperfusion are not benign, and include shock, acidosis, rhabdomyolysis, and renal failure. For those with advanced limb ischemia, the need to amputate may remain despite reperfusion. Aggressive pursuit of fasciotomies after reperfusion are prudent to relieve or avoid development of compartment syndrome and to assess the viability of the muscle.
Hemodynamically stable ATAAD with isolated and advanced limb malperfusion as the presenting feature may benet from prioritizing limb reperfusion with a brief period of recovery before central aortic repair [38]. For ATAAD patients with mul­tiple vascular beds affected by malperfusion, and for those with isolated early peripheral MPS, our preference is for immediate central aortic repair. Several stud­ies report favorable results with immediate proximal aortic repair alone relieving lower limb ischemia in 60–100% of patients [5, 4648]. After central repair, intra­operative recognition of ongoing limb ischemia and expeditious revascularization produces excellent outcomes comparable to those of ATAAD patients without mal­perfusion syndromes [43].
Conclusions
The ideal approach to the patient with ATAAD and malperfusion includes rapid diagnosis and reperfusion of the ischemic vascular beds while minimizing the risk of aortic rupture. In cases where there is radiographic and clinical evidence of multi­organ malperfusion, or with ongoing hemodynamic instability, an aortic repair rst strategy optimizes the timing of true lumen reperfusion throughout the aorta and eliminates the risk of rupture and inuence of pericardial tamponade. However, when advanced single organ malperfusion syndromes are present (excluding coro­nary malperfusion), there may be opportunities to avoid the additional metabolic and inammatory insult of open surgery by utilizing a percutaneous revasculariza­tion rst approach. The operative mortality with all approaches remains disappoint­ingly high but a gratifying rate of salvage can be anticipated when patients are triaged quickly to centers and surgeons with extensive experience caring for a wide variety of aortic pathology.
Conicts No conicts of interest to report.
Funding No outside funding received.
Management of Complicated Type A Aortic Dissection: The Cornell-New York…
https://t.me/med1917
361
References
1. Berretta P, Patel HJ, Gleason TG, Sundt TM, Myrmel T, Desai ND, etal. IRAD experience on
surgical type A acute dissection patients: results and predictors of mortality. Ann Cardiothorac Surg. 2016.
2. Conzelmann LO, Weigang E, Mehlhorn U, Abugameh A, Hoffmann I, Blettner M, et al.
Mortality in patients with acute aortic dissection type A: analysis of pre- and intraoperative risk factors from the German Registry for Acute Aortic Dissection Type A (GERAADA). Eur J Cardiothorac Surg. 2016;49:e44–52.
3. Zindovic I, Gudbjartsson T, Ahlsson A, Fuglsang S, Gunn J, Hansson EC, etal. Malperfusion
in acute type A aortic dissection: an update from the Nordic Consortium for Acute Type A Aortic Dissection. J Thorac Cardiovasc Surg. 2019;157:1324–1333.e6.
4. Czerny M, Schoenhoff F, Etz C, Englberger L, Khaladj N, Zierer A, et al. The impact of
pre-operative malperfusion on outcome in acute type A aortic dissection: results from the GERAADA Registry. J Am Coll Cardiol. 2015;65:2628–35.
5. Girardi LN, Krieger KH, Lee LY, Mack CA, Tortolani AJ, Isom OW.Management strate-
gies for type A dissection complicated by peripheral vascular malperfusion. Ann Thorac Surg. 2004;77:1309–14; discussion 1314.
6. Fann JI, Sarris GE, Mitchell RS, Shumway NE, Stinson EB, Oyer PE, etal. Treatment of
patients with aortic dissection presenting with peripheral vascular complications. Ann Surg. 1990;212:705–13.
7. Debakey ME, Henly WS, Cooley DA, Morris GC, Crawford ES, Beall AC.Surgical manage-
ment of dissecting aneurysms of the aorta. J Thorac Cardiovasc Surg. 1965;49:130–49.
8. Daily PO, Trueblood HW, Stinson EB, Wuerein RD, Shumway NE.Management of acute
aortic dissections. Ann Thorac Surg. 1970;10:237–47.
9. Augoustides JGT, Geirsson A, Szeto WY, Walsh EK, Cornelius B, Pochettino A, et al.
Observational study of mortality risk stratication by ischemic presentation in patients with acute type A aortic dissection: the Penn classication. Nat Clin Pract Cardiovasc Med. 2009;6:140–6.
10. Olsson C, Hillebrant C-G, Liska J, Lockowandt U, Eriksson P, Franco-Cereceda A.Mortality
in acute type A aortic dissection: validation of the Penn classication. Ann Thorac Surg. 2011;92:1376–82.
11. Chien T-M, Cheng Q-H, Chen C-W, Yu C-P, Chen H-M, Chen Y-F.Modication of Penn clas-
sication and its validation for acute type A aortic dissection. Am J Cardiol. 2014;114:497–9.
12. Ghoreishi M, Wise ES, Croal-Abrahams L, Tran D, Pasrija C, Drucker CB, etal. A novel risk
score predicts operative mortality after acute type A aortic dissection repair. Ann Thorac Surg. 2018;106:1759–66.
13. Yang B, Patel HJ, Williams DM, Dasika NL, Deeb GM.Management of type A dissection with
malperfusion. Ann Cardiothorac Surg. 2016;5:265–74.
14. Williams DM, Lee DY, Hamilton BH, Marx MV, Narasimham DL, Kazanjian SN, etal. The
dissected aorta: percutaneous treatment of ischemic complications–principles and results. J Vasc Interv Radiol. 1997;8:605–25.
15. Kamman AV, Yang B, Kim KM, Williams DM, Michael Deeb G, Patel HJ.Visceral malp-
erfusion in aortic dissection: the Michigan experience. Semin Thorac Cardiovasc Surg. 2017;29:173–8.
16. Goldberg JB, Lansman SL, Kai M, Tang GHL, Malekan R, Spielvogel D.Malperfusion in type
A dissection: consider reperfusion rst. Semin Thorac Cardiovasc Surg. 2017;29:181–5.
17. Berretta P, Trimarchi S, Patel HJ, Gleason TG, Eagle KA, Di Eusanio M.Malperfusion syn-
dromes in type A aortic dissection: what we have learned from IRAD.J Vis Surg. 2018;4:65.
18. Sandhu HK, Charlton-Ouw KM, Jeffress K, Leake S, Perlick A, Miller CC, etal. Risk of
mortality after resolution of spinal malperfusion in acute dissection. Ann Thorac Surg. 2018;106:473–81.
362
https://t.me/med1917
19. Mehta RH, Suzuki T, Hagan PG, Bossone E, Gilon D, Llovet A, etal. Predicting death in
patients with acute type a aortic dissection. Circulation. 2002;105:200–6.
20. Neri E, Toscano T, Papalia U, Frati G, Massetti M, Capannini G, etal. Proximal aortic dis-
section with coronary malperfusion: presentation, management, and outcome. J Thorac Cardiovasc Surg. 2001;121:552–60.
21. Kreibich M, Bavaria JE, Branchetti E, Brown CR, Chen Z, Khurshan F, etal. Management of
patients with coronary artery malperfusion secondary to type A aortic dissection. Ann Thorac Surg. 2019;107:1174–80.
22. Eren E, Toker ME, Tunçer A, Keles C, Erdogan HB, Anasiz H, etal. Surgical management of
coronary malperfusion due to type A aortic dissection. J Card Surg. 2007;22:2–6.
23. Kawahito K, Adachi H, Murata S, Yamaguchi A, Ino T.Coronary malperfusion due to type A
aortic dissection: mechanism and surgical management. Ann Thorac Surg. 2003;76:1471–6; discussion 1476.
24. Stanger O, Schachner T, Gahl B, Oberwalder P, Englberger L, Thalmann M, et al. Type A
aortic dissection after nonaortic cardiac surgery. Circulation. 2013;128:1602–11.
25. Yang B, Norton EL, Hobbs R, Farhat L, Wu X, Hornsby WE, et al. Short- and long-term
outcomes of aortic root repair and replacement in patients undergoing acute type A aortic dis­section repair: twenty-year experience. J Thorac Cardiovasc Surg. 2019;157:2125–36.
26. Bavaria JE, Brinster DR, Gorman RC, Woo YJ, Gleason T, Pochettino A.Advances in the treat-
ment of acute type A dissection: an integrated approach. Ann Thorac Surg. 2002;74:S1848–52; discussion S1857.
27. Lau C, Wingo M, Rahouma M, Ivascu N, Iannacone E, Kamel M, etal. Valve-sparing root
replacement in patients with bicuspid aortopathy: an analysis of cusp repair strategy and valve durability. J Thorac Cardiovasc Surg. 2019.
28. Estrera AL, Garami Z, Miller CC, Porat EE, Achouh PE, Dhareshwar J, etal. Acute type A
aortic dissection complicated by stroke: can immediate repair be performed safely? J Thorac Cardiovasc Surg. 2006;132:1404–8.
29. Di Eusanio M, Patel HJ, Nienaber CA, Montgomery DM, Korach A, Sundt TM, etal. Patients
with type A acute aortic dissection presenting with major brain injury: should we operate on them? J Thorac Cardiovasc Surg. 2013;145:S213–21.e1.
30. Urbanski PP, Wagner M.Perfusion and repair technique in acute aortic dissection with cerebral
malperfusion and damage of the innominate artery. J Thorac Cardiovasc Surg. 2012;144:982–4.
31. Heran MKS, Balaji N, Cook RC. Novel percutaneous treatment of cerebral malperfusion
before surgery for acute type A dissection. Ann Thorac Surg. 2019;108:e15–7.
32. Sultan I, Bianco V, Patel HJ, Arnaoutakis GJ, Di Eusanio M, Chen EP, etal. Surgery for type A
aortic dissection in patients with cerebral malperfusion: results from the International Registry of Acute Aortic Dissection. J Thorac Cardiovasc Surg. 2019.
33. Frederick JR, Yang E, Trubelja A, Desai ND, Szeto WY, Pochettino A, etal. Ascending aortic
cannulation in acute type a dissection repair. Ann Thorac Surg. 2013;95:1808–11.
34. Hameed I, Rahouma M, Khan FM, Wingo M, Demetres M, Tam DY, etal. Cerebral protection
strategies in aortic arch surgery: a network meta-analysis. J Thorac Cardiovasc Surg. 2019.
35. Morimoto N, Okada K, Okita Y.Lack of neurologic improvement after aortic repair for acute
type A aortic dissection complicated by cerebral malperfusion: predictors and association with survival. J Thorac Cardiovasc Surg. 2011;142:1540–4.
36. Di Eusanio M, Trimarchi S, Patel HJ, Hutchison S, Suzuki T, Peterson MD, etal. Clinical pre-
sentation, management, and short-term outcome of patients with type A acute dissection com­plicated by mesenteric malperfusion: observations from the International Registry of Acute Aortic Dissection. J Thorac Cardiovasc Surg. 2013;145:385–390.e1.
37. Yang B, Norton EL, Rosati CM, Wu X, Kim KM, Khaja MS, etal. Managing patients with
acute type A aortic dissection and mesenteric malperfusion syndrome: a 20-year experience. J Thorac Cardiovasc Surg. 2019;158:675–687.e4.
38. Yang B, Rosati CM, Norton EL, Kim KM, Khaja MS, Dasika N, etal. Endovascular fenestra-
tion/stenting rst followed by delayed open aortic repair for acute type A aortic dissection with malperfusion syndrome. Circulation. 2018;138:2091–103.
E. Iannacone et al.
Management of Complicated Type A Aortic Dissection: The Cornell-New York…
https://t.me/med1917
39. Patel HJ, Williams DM, Dasika NL, Suzuki Y, Deeb GM.Operative delay for peripheral malp-
erfusion syndrome in acute type A aortic dissection: a long-term analysis. J Thorac Cardiovasc Surg. 2008;135:1288–95; discussion 1295.
40. Yamashiro S, Arakaki R, Kise Y, Inafuku H, Kuniyoshi Y. Management of visceral malp-
erfusion complicated with acute type A aortic dissection. Interact Cardiovasc Thorac Surg. 2015;21:346–51.
41. Tsagakis K, Konorza T, Dohle DS, Kottenberg E, Buck T, Thielmann M, etal. Hybrid operat-
ing room concept for combined diagnostics, intervention and surgery in acute type A dissec­tion. Eur J Cardiothorac Surg. 2013;43:397–404.
42. Girardi LN. Commentary: Acute type A aortic dissection and mesenteric malperfusion syn-
drome: still a long way to go. J Thorac Cardiovasc Surg. 2019;158:688–9.
43. Preece R, Srivastava V, Akowuah E, Kendall S. Should limb revascularization take priority
over dissection repair in type A aortic dissection presenting as isolated acute limb ischaemia. Interact Cardiovasc Thorac Surg. 2017;25:643–6.
44. Rutherford RB, Baker JD, Ernst C, Johnston KW, Porter JM, Ahn S, et al. Recommended
standards for reports dealing with lower extremity ischemia: revised version. J Vasc Surg. 1997;26:517–38.
45. Currie IS, Wakelin SJ, Lee AJ, Chalmers RT.Plasma creatine kinase indicates major amputa-
tion or limb preservation in acute lower limb ischemia. J Vasc Surg. 2007;45:733–9.
46. Charlton-Ouw KM, Sritharan K, Leake SS, Sandhu HK, Miller CC, Azizzadeh A, et al.
Management of limb ischemia in acute proximal aortic dissection. J Vasc Surg. 2013;57:1023–9.
47. Charlton-Ouw KM, Sandhu HK, Leake SS, Jeffress K, Miller CC, Durham CA, etal. Need
for limb revascularization in patients with acute aortic dissection is associated with mesenteric ischemia. Ann Vasc Surg. 2016;36:112–20.
48. Girdauskas E, Kuntze T, Borger MA, Falk V, Mohr F-W.Surgical risk of preoperative malper-
fusion in acute type A aortic dissection. J Thorac Cardiovasc Surg. 2009;138:1363–9.
363
Management ofComplicated Acute
https://t.me/med1917
Type A Aortic Dissection: The Stanford Approach
AlbertJ.Pedroza andMichaelP.Fischbein
Introduction
Acute aortic dissection is a rare, life-threatening condition with an incidence rang­ing from 5 to 10/100,000 person-years [1]. Cardiac surgeons have long recognized that this disease process is clinically challenging with a high mortality rate. Among the simplest and earliest classication systems, the Stanford paradigm proposed in 1970 by Dailey etal. established surgical repair as the standard of care for the ‘Type A’ variant involving the ascending aorta (Fig.1) [2]. While the wealth of experience treating this entity over the subsequent ve decades has reafrmed the need for prompt surgical intervention, one central theme remains certain: not all aortic dis­sections are created equal. Within the cohort of patients referred for prompt surgical repair of acute type A aortic dissection (ATAAD), many potential complicating fac­tors contribute to operative candidacy, optimal interventional strategy and morbid­ity/mortality risk. In particular, the presence of neurologic injury, mesenteric malperfusion, limb ischemia or shock mandate rapid decisive action. When present, these factors comprise a heterogeneous “complicated ATAAD” variant with height­ened technical challenges and surgical risk. Whereas the debate around neurologic status reects a question of ‘if’ an operation should be attempted, the presence of malperfusion or limb ischemia raises important considerations of ‘how’ it should be performed. Various institutional paradigms have been built around theories on opti­mal management, reecting the lack of clear consensus across the specialty about how to optimally manage these difcult problems. The growing body of literature surrounding complicated aortic dissection management underscores the need for centralized cardiac surgery referral centers capable of interdisciplinary aortic inter­ventions and the rapidly evolving practice of the modern aortic surgeon. This chap­ter presents pertinent lessons learned from institutional experience and multi-center
A. J. Pedroza · M. P. Fischbein (*) Cardiothoracic Surgery, Stanford University, Stanford, CA, USA e-mail: alpedroz@stanford.edu; mschbe@stanford.edu
J. S. Coselli et al. (eds.), Aortic Dissection and Acute Aortic Syndromes,
https://doi.org/10.1007/978-3-030-66668-2_26
365© Springer Nature Switzerland AG 2021
366
Stanford Classification
https://t.me/med1917
Fig. 1 Stanford classication for acute aortic dissection. In the “Type A” variant, the primary intimal tear occurs in the ascending aortic segment, while in “Type B”, the tear occurs distal to the aortic arch, affecting the descending thoracic aorta
Type A Type B
A. J. Pedroza and M. P. Fischbein
databases to highlight branch points in the treatment algorithm for compli­cated ATAAD.
Pre-Operative Evaluation
Operative Candidacy
Decisions on operative candidacy for ATAAD in general are made difcult by the very poor outcomes of medical management alone. While modern mortality esti­mates for medical management alone are implicitly limited by selection and report­ing biases, data from the International Registry of Acute Aortic Dissection (IRAD) database showed 57% mortality for patients treated medically. Surgical outcomes have steadily improved since the inception of the IRAD database with reported multi-center surgical mortality rates falling from 25% to 18% between 1995 and 2013 [3]. Findings from the IRAD database also highlight age-dependent increases in mortality risk regardless of treatment modality but consistent superiority of surgi­cal treatment up to 80years of age [4]. The paucity of data for patients over 80 within this cohort precludes robust determination of optimal management for octo­genarians. Given these dichotomous outcomes, every ATAAD patient should be considered for operative repair. With few exceptions, our default pathway is imme­diate transfer directly to a hybrid operating room and preparation for central aortic repair. The presence of distal malperfusion, which may affect one or multiple organ beds, represents a central branch point in treatment algorithm for patients present­ing with ATAAD.