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References
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References
1. Illig KA, Donahue D, Duncan A, Freischlag J, Gelabert H, Johansen K, Jordan S, Sanders R, Thompson R.Reporting standards of the Society for Vascular Surgery for thoracic outlet syndrome. J Vasc Surg. 2016a;64:e23–35.
2. Illig KA, Donahue D, Duncan A, Freischlag J, Gelabert H, Johansen K, Jordan S, Sanders R, Thompson R.Reporting standards of the Society for Vascular Surgery for thoracic outlet syndrome: executive summary. J Vasc Surg. 2016b;64:797–802.
3. Expert Panels on Vascular Imaging, Thoracic Imaging, and Neurological Imaging, Zurkiya O, Ganguli S, Kalva SP, etal. ACR appropriateness criteria® thoracic outlet syndrome. J Am Coll Radiol. 2020;17(5S):S323–34.
4. Yin ZG, Gong KT, Zhang JB.Outcomes of surgical management of neurogenic thoracic out­let syndrome: a systematic review and Bayesian perspective. J Hand Surg Am. 2019;44:416. e1–416.e17.
5. Blondin M, Garner GL, Hones KM, Nichols DS, Cox EA, Chim H.Considerations for sur­gical treatment of neurogenic thoracic outlet syndrome: a meta-analysis of patient-reported outcomes. J Hand Surg Am. 2023;48:585–94.
6. Karaolanis G, Antonopoulos CN, Koutsias SG, Giosdekos A, Metaxas EK, Tzimas P, de Borst GJ, Geroulakos G. A systematic review and meta-analysis for the management of Paget­Schroetter syndrome. J Vasc Surg Venous Lymphat Disord. 2021;9:801–10.
7. Illig KA, Rodriguez-Zoppi E.How common is thoracic outlet syndrome? Thorac Surg Clin. 2021;31:11–7.
8. George EL, Arya S, Rothenberg KA, Hernandez-Boussard T, Ho VT, Stern JR, Gelabert HA, Lee JT.Contemporary practices and complications of surgery for thoracic outlet syndrome in the United States. Ann Vasc Surg. 2021;72:147–58.
9. Jubbal KT, Zavlin D, Harris JD, Liberman SR, Echo A.Morbidity of rst rib resection in the surgical repair of thoracic outlet syndrome. Hand (N Y). 2019;14:636–40.
10. Pesser N, Bode A, Goeteyn J, Hendriks J, van Nuenen BFL, Illig KA, van Sambeek MRHM, Teijink JAW. Surgical management of post-thrombotic syndrome in chronic venous thoracic outlet syndrome. J Vasc Surg Venous Lymphat Disord. 2021a;9:1159–67.
11. Bozzay JD, Walker PF, Ronaldi AE, Patel JA, Koelling EE, White PW, Rasmussen TE, Golarz SR, White JM.Infraclavicular thoracic outlet decompression compared to supraclavicular tho­racic outlet decompression for the management of venous thoracic outlet syndrome. Ann Vasc Surg. 2020;65:90–9.
12. Dua A, Rothenberg KA, Gologorsky RC, Deslarzes-Dubuis C, Lee JT.Long-term quality of life comparison between supraclavicular and infraclavicular rib resection in patients with vTOS.Ann Vasc Surg. 2020a;62:128–32.
13. Dua A, Deslarzes-Dubuis C, Rothenberg KA, Gologorsky R, Lee JT. Long-term func­tional outcomes follow-up after 188 rib resections in patients with TOS.Ann Vasc Surg. 2020b;68:28–33.
14. Silverberg D, Fish M, Lubetsky A, Rimon U, Raskin D, Greenberg G, Halak M.Long-term outcome after nonsurgical management of Paget-Schroetter syndrome. J Vasc Surg Venous Lymphat Disord. 2021;9:170–7.
15. Balderman J, Abuirqeba AA, Eichaker L, Pate C, Earley JA, Bottros MM, Jayarajan SN, Thompson RW. Physical therapy management, surgical treatment, and patient-reported out­comes measures in a prospective observational cohort of patients with neurogenic thoracic outlet syndrome. J Vasc Surg. 2019;70:832–41.
16. Pesser N, Goeteyn J, van der Sanden L, Houterman S, van Alfen N, van Sambeek MRHM, van Nuenen BFL, Teijink JAW.Feasibility and outcomes of a multidisciplinary care pathway for neurogenic thoracic outlet syndrome: a prospective observational cohort study. Eur J Vasc Endovasc Surg. 2021b;61:1017–24.
17. Johansen K.Rib-sparing scalenectomy for neurogenic thoracic outlet syndrome: early results. J Vasc Surg. 2021;73:2059–63.
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18. Ruopsa N, Ristolainen L, Vastamäki M, Vastamäki H. Neurogenic thoracic outlet syndrome with supraclavicular release: long-term outcome without rib resection. Diagnostics (Basel). 2021;11:450.
19. Panda N, Phillips WW, Geller AD, Lipsitz S, Colson YL, Donahue DM. Supraclavicular approach for neurogenic thoracic outlet syndrome: description of a learning curve. Ann Thorac Surg. 2021;112:1616–23.
20. Goeteyn J, Pesser N, Houterman S, van Sambeek MRHM, van Nuenen BFL, Teijink JAW.Surgery versus continued conservative treatment for neurogenic thoracic outlet syn­drome: the rst randomised clinical trial (STOPNTOS-trial). Eur J Vasc Endovasc Surg. 2022a;64:119–27.
21. Goeteyn J, Van Der Sanden L, Pesser N, Houterman S, van Sambeek MRHM, van Nuenen BFL, Teijink JAW.Redo surgery for neurogenic thoracic outlet syndrome is useful. J Vasc Surg. 2022b;76:531–7.
22. Pantoja JL, Rigberg DA, Gelabert HA.The evolving role of endovascular therapy in the man­agement of arterial thoracic outlet syndrome. J Vasc Surg. 2022;75:968–75.
23. Stilo F, Montelione N, Benedetto F, Spinelli D, Vigliotti RC, Spinelli F.Thirty-year experience of transaxillary resection of rst rib for thoracic outlet syndrome. Int Angiol. 2020;39:82–8.
24. Moridzadeh RS, Gelabert MC, Rigberg DA, Gelabert HA.A novel technique for transaxil­lary resection of fully formed cervical ribs with long-term clinical outcomes. J Vasc Surg. 2021;73:572–80.
25. Martinez BD, Albeshri H, Chulkov M, Alharthi S, Nazzal MMS, Sferra J. Development and evolution of a robotic surgical technique for the treatment of thoracic outlet syndrome. J Vasc Surg. 2021;74:938–45.
26. Donahue DM, Godoy IRB, Gupta R, Donahue JA, Torriani M.Sonographically guided botu­linum toxin injections in patients with neurogenic thoracic outlet syndrome: correlation with surgical outcomes. Skelet Radiol. 2020;49:715–22.
2 Thoracic-Outlet-Syndrome
Chapter 3
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Distal Aortic Dissection Type Stanford B
3.1 Guidelines
3.1.1 Denition andClassication
Acute type B aortic dissection (ATBAD) is the result of a tear in the intimal arterial layer, which allows blood to propagate within the medial layer. This creates a ap, which divides the aorta into a true lumen (TL), and a false lumen (FL). The most common site for the proximal intimal tear in ATBAD is located just distal to the origin of the left subclavian artery. In 90% of cases, ATBAD has a secondary tear that allows blood to re-enter the TL at what is known as the re-entry site [1].
There are 2 commonly used anatomic classication systems for aortic dissection,
the DeBakey system and the Stanford system [2].
The DeBakey system categorizes dissections into types I, II, and III, based on the
origin of the intimal tear and the extent of the dissection:
• Type I: Dissection tear originates in the ascending aorta and propagates distally
to include the aortic arch and typically the descending aorta.
• Type II: Dissection tear is conned only to the ascending aorta.
• Type III: Dissection tear originates in the descending thoracic aorta and propa-
gates most often distally.
– Type IIIa: Dissection tear is conned only to the descending thoracic aorta. – Type IIIb: Dissection tear originates in the descending thoracic aorta and
extends below the diaphragm. The Stanford classication system divides dissections into 2 categories according to whether the ascending aorta is involved or not, regardless of the site of origin:
• Type A: All dissections involving the ascending aorta, irrespective of the site of
the intimal tear.
Switzerland AG 2023 E. S. Debus, R. T. Grundmann, Evidence-based Therapy in Vascular Surgery,
https://doi.org/10.1007/978-3-031-47397-5_3
47© The Author(s), under exclusive license to Springer Nature
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3 Distal Aortic Dissection Type Stanford B
• Type B: All dissections that do not involve the ascending aorta (including dissec-
tions that involve the aortic arch but spare the ascending aorta).
The European Association for Cardio-Thoracic Surgery and the European Society for Vascular Surgery published an expert consensus document [3], in which they added a third category called “non-A-non-B dissection,” to be used for patients whose proximal dissection ap begins in the aortic arch.
The International Registry of Acute Aortic Dissection (IRAD) proposed that aor­tic dissection be divided into 4 temporal types based on time of symptom onset [4]: hyperacute (symptom onset to 24h), acute (2–7days), subacute (8–30days), and chronic (>30days). The most contemporary temporal classication system divides [2]: hyperacute (time from onset of symptoms <24h, acute 1–14 days, subacute 15–90days, chronic >90days).
3.1.2 2022 ACC/AHA Guideline fortheDiagnosis
andManagement ofAortic Disease
The American Heart Association/American College of Cardiology practice guide­lines recommend [2]:
3.1.2.1 Management ofAcute Type B Aortic Dissection
• In all patients with uncomplicated acute type B aortic dissection, medical ther-
apy is recommended as the initial management strategy. (Class of recommenda-
tion [COR] 1; Level of evidence [LOE] B-NR).
• In patients with acute type B aortic dissection and rupture or other complications
(Table3.1), intervention is recommended. (COR 1; LOE C-LD).
Table 3.1 Consensus features of complicated acute type B aortic dissection [2]
Feature Comment
Aortic rupture This can be either free or contained (including hemothorax, increasing
periaortic hematoma, or both; or mediastinal hematoma) and should be addressed promptly
Branch artery occlusion and malperfusion
Extension of dissection Extension of the dissection ap either distally or proximally (ie,
Aortic enlargement Progressive enlargement of the true, false, or both lumens while in the
Intractable pain Uncontrolled
hypertension
Complete or partial occlusion of a major branch, with or without clinical evidence of ischemia; this includes visceral, renal, and peripheral arterial branches
retrograde type A dissection)
acute phase may require prompt intervention
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Table 3.2 High-risk features in uncomplicated acute type B aortic dissection [2]
High-risk imaging ndings
• Maximal aortic diameter>40mm
• False-lumen diameter>20–22mm
• Entry tear >10mm
• Entry tear on lesser curvature
• Increase in total aortic diameter of >5mm between serial imaging studies
• Bloody pleural effusion
• Imaging-only evidence of malperfusion
High-risk clinical ndings
• Refractory hypertension despite >3 different classes of antihypertensive medications at maximal recommended or tolerated doses
• Refractory pain persisting >12h despite maximal recommended or tolerated doses
• Need for readmission
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• In patients with rupture, in the presence of suitable anatomy, endovascular stent grafting, rather than open surgical repair, is recommended. (COR 1; LOE C-EO).
• In patients with other complications, in the presence of suitable anatomy, the use of endovascular approaches, rather than open surgical repair, is reasonable. (COR 2a; LOE C-LD).
• In patients with uncomplicated acute type B aortic dissection who have high-risk anatomic features (Table 3.2), endovascular management may be considered. (COR 2b; LOE B-R).
(Note: R Randomized; NR Nonrandomized; LD Limited Data; EO Expert
Opinion)
3.1.3 Clinical Practice Guidelines oftheEuropean Society
forVascular Surgery (ESVS)
The following recommendations for the management of acute type B aortic dissec­tions are given [1]:
• Recommendation 12: Patients with acute type B aortic dissection who develop new or recurrent abdominal pain and where there is any suspicion of visceral, renal and/or limb malperfusion should undergo repeat CT imaging. (Class I/ Level of Evidence C).
• Recommendation 13: Medical therapy should always be part of the treatment of patients with acute type B dissection. (Class I/Level of evidence C).
• Recommendation 14: In patients with acute type B aortic dissection, β-blockers should be considered as the rst line of medical therapy. (Class IIa/Level of evi­dence C).
• Recommendation 15: In patients with acute type B aortic dissection who do not respond or are intolerant of β-blockers, calcium channel antagonists and/or
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3 Distal Aortic Dissection Type Stanford B
renin-angiotensin inhibitors may be considered as alternatives or complementa­ries. (Class IIb/Level of evidence C).
• Recommendation 16: In patients with complicated acute type B aortic dissec­tion, endovascular repair with thoracic endografting should be the rst line inter­vention. (Class I/Level of Evidence C).
• Recommendation 17: In complicated acute type B aortic dissection, endovascu­lar fenestration should be considered to treat malperfusion. (Class IIa/Level of evidence C).
• Recommendation 18: To prevent aortic complications in uncomplicated acute type B aortic dissection, early thoracic endografting may be considered selec­tively. (Class IIb/Level of evidence B).
• Recommendation 19: In acute complicated type B aortic dissection, open repair should be considered as an alternative to endovascular therapy following failure of endovascular management or where endovascular interventions are contrain­dicated. (Class IIa/Level of evidence C).
Regarding chronic dissection, it is recommended:
• Recommendation 33: In patients with chronic aortic dissection and acute aortic symptoms, emergency repair should be considered if malperfusion, rupture, or progression of dissection is conrmed on imaging. (Class IIa/Level of Evidence C).
• Recommendation 34a: In patients with chronic aortic dissection, a descending thoracic aortic diameter between 56 to 59mm may be considered as an indica­tion for treatment in patients at reasonable surgical risk. (Class IIb/Level of evi­dence C).
• Recommendation 34b: In patients with chronic aortic dissection, a descending thoracic aortic diameter greater than 60mm should be considered as an indica­tion for treatment in patients at reasonable surgical risk. (Class IIa/Level of evi­dence C).
• Recommendation 35: In patients with chronic aortic dissection and thoraco­abdominal extension, an aortic diameter greater than 60mm should be consid­ered as an indication for treatment in patients at reasonable surgical risk. (Class IIa/Level of evidence C).
• Recommendation 36: Open repair of aneurysmal or symptomatic chronic type B aortic dissection in patients with low surgical risk should be considered in dedi­cated centres with low complication rates. (Class IIa/Level of evidence C).
• Recommendation 37: In patients with chronic type B dissection undergoing operative repair, intra-procedural cerebrospinal uid drainage, left heart bypass, and moderate hypothermia should be considered to reduce procedural mortality and spinal cord injury. (Class IIa/Level of Evidence C).
• Recommendation 38: In patients with moderate to high surgical risk or with contraindications to open repair, endovascular repair of complicated chronic type B aortic dissection should be considered in dedicated centres. (Class IIa/Level of evidence C).
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• Recommendation 39: In patients at risk of further aortic complications with suit­able anatomy for endografting, endovascular repair of uncomplicated chronic type B aortic dissections should be considered in the sub-acute phase, in dedi­cated centres. (Class IIa/Level of evidence B).
3.1.3.1 Acute Aortic Syndromes
Acute aortic syndromes (AAS) consist of three interrelated diseases: aortic dissec­tion, penetrating aortic ulcer (PAU), and intramural haematoma (IMH). There are few details on the latter two entities in the ESVS guidelines because the evidence base for treatment is small. The recommendations are [1]:
• Recommendation 20: Uncomplicated type B intramural haematoma and pene­trating aortic ulcer should be treated medically, and followed by serial imaging surveillance. (Class I/Level of evidence C) [Uncomplicated/complicated intra­mural haematoma means absence or presence of recurrent pain, expansion of the intramural haematoma, peri-aortic haematoma, and intimal disruption].
• Recommendation 21: Endovascular repair should be considered for complicated intramural haematoma type B. (Class IIa/Level of evidence C).
• Recommendation 22: Endovascular repair should be considered for complicated penetrating aortic ulcer type B. (Class IIa/Level of evidence C) [Complicated penetrating aortic ulcer (PAU) means presence of recurrent pain or PAU that initially measures >20mm in diameter or> 10mm in depth or progression of total aortic diameter].
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3.1.4 Society ofThoracic Surgeons/American Association
forThoracic Surgery
The practice guidelines on the management of type B aortic dissection state [5]:
3.1.4.1 Acute Complicated Type B Aortic Dissection (TBAD)
• TEVAR (thoracic endovascular aortic repair) is indicated for complicated hyper­acute, acute, or subacute TBADs with rupture and/or malperfusion and favour­able anatomy for TEVAR (Class of Recommendation [COR] I/Level of Evidence [LOE] B-nonrandomised [NR]).
• Open surgical repair for complicated hyperacute, acute, or subacute TBADs should be considered for those patients with unsuitable anatomy for TEVAR (COR IIA/LOE B/NR).
• Fenestration may be considered for complicated hyperacute, acute, or subacute TBADs (COR IIB/LOE C/LD [limited data]).
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3 Distal Aortic Dissection Type Stanford B
3.1.4.2 Uncomplicated TBAD
• A stepwise approach to the evaluation and treatment of acute/subacute uncom­plicated TBAD should be applied that includes identication of the primary entry tear site location, dening the proximity and distance of the dissection to the LSA [left subclavian artery], calibration of the maximum orthogonal aortic diameter, and conrmation of the lack of any organ malperfusion or other indica­tions of complicated disease (COR I/LOE B-NR).
• Optimal medical therapy (OMT) is the recommended treatment for patients with uncomplicated TBAD (COR I/LOE B-NR).
• Prophylactic TEVAR may be considered in patients with uncomplicated TBAD to reduce late aortic-related adverse events and aortic-related death. (COR II B/ LOE B-NR). [see Table3.3 for details].
• Close clinical follow-up after hospital discharge is recommended for patients presenting with acute TBAD (COR I/LOE B-NR).
3.1.4.3 Chronic TBAD
• Open surgical repair should be considered for patients with chronic TBAD with indications for intervention, unless comorbidities are prohibitive or anatomy is not suitable for TEVAR (COR II A/LOE B-NR).
• TEVAR is reasonable for patients with chronic TBAD with an indication for intervention with suitable anatomy (adequate landing zone, absence of ascend­ing or arch aneurysm) but who are at high risk for complications of open repair due to comorbidities (COR II A/LOE B-NR).
• TEVAR alone as sole therapy is not recommended in patients with chronic TBAD who have a large abdominal aortic aneurysm [AAA], an inadequate distal landing zone, and/or large distal reentry tears (COR III: no benet/LOE C-LD).
Table 3.3 Morphological features posing high risk of late sequelae
– Primary entry tear at greater curve of distal arch
– Short proximity of entry tear to left subclavian artery ostium
– Initial aortic diameter≥40mm – Initial false lumen diameter≥22mm – Number/size of fenestrations between
true and false lumen – Stent graft-induced new entry – Partial false lumen thrombosis
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3.1.4.4 Timing ofIntervention
• In patients with acute uncomplicated TBAD with high-risk features, it may be reasonable to consider delaying treatment (beyond 24 h up to 90 days) with TEVAR to reduce early adverse events and to improve late outcomes (COR II B/ LOE C-LD).
3.1.4.5 Connective Tissue Disorders
• Open surgical repair over TEVAR is reasonable for more durable treatment in patients with connective tissue disorders and TBAD who have progression of disease despite OMT (COR I/LOE B-NR).
• TEVAR is reasonable in patients with connective tissue disorders with acute complicated TBADs and anatomy favourable for TEVAR as a bridge to delayed open reconstruction (COR IIA LOE C-LD).
3.1.4.6 Spinal Cord Protection Adjuncts toTEVAR
• Revascularisation (open surgical or endovascular) of the left subclavian artery after TEVAR coverage that obstructs antegrade LSA ow is recommended to decrease the risk of spinal cord ischaemia [SCI] (COR I/LOE B-NR).
• It is reasonable to establish CSF drainage in type B dissection patients undergo­ing TEVAR if they are at increased risk for spinal cord ischaemia (eg, coverage >20cm or within 2cm of the celic artery origin or other risk factors) and time permits (i.e., nonemergent circumstances) (COR IIA/LOE B-NR).
• It is reasonable to establish CSF drainage in type B dissection patients who develop symptoms of paraparesis/paraplegia (COR IIA/LOE B-NR).
3.1.4.7 Management ofTBAD withArch Involvement
• OMT is reasonable in patients with uncomplicated TBAD and retrograde dissec­tion from a tear at or distal to the left subclavian artery as long as retrograde extension is limited to the arch (zones 1 and 2) (COR IIA/LOE C-LD).
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3 Distal Aortic Dissection Type Stanford B
3.2 Meta-Analyses/Systematic Reviews
3.2.1 Acute andSubacute Uncomplicated Type B Aortic
Dissection: BMT vs. TEVAR
Hossack etal. [6] reviewed systematically the evidence in patients with acute or subacute uncomplicated TBAD (uTBAD) treated by either TEVAR and best medi­cal therapy (BMT) or BMT alone, to see whether TEVAR improved early and late all cause and aorta related mortality. 6 studies encompassing 14,706 patients (including 1066 TEVARs) were included in this meta-analysis. Early mortality after BMT was calculated to be 7.4% overall, and 6.2% after EVAR (no signicant advantage of TEVAR for early mortality). There were no statistically signicant differences between TEVAR and BMT with regards to inpatient mortality, early re­intervention by TEVAR or surgery. BMT was associated with a signicantly lower risk of early stroke (p=.002), whereas the risk of late all cause (HR 1.54, 95% CI
1.27–1.86, p < .001) and aorta related mortality (HR 2.71, 95% CI 1.49–4.94,
p=.001) was signicantly higher than with TEVAR.No suitable data regarding late aortic re-intervention was found for meta-analysis. Based on the limited data and studies, the authors concluded that it remains uncertain whether TEVAR is bene­cial in the management of acute/subacute uTBAD.
A second meta-analysis by Wang etal. [7] came to a different conclusion. These
authors compared best medical therapy (BMT) with BMT + TEVAR in acute uncomplicated Stanford TBAD based on 7 observational studies and two ran­domised controlled trials with a total of 15,066 patients. There were no signicant differences in early outcomes (aortic rupture, retrograde dissection, paraplegia/ paraparesis, reintervention and mortality) between TEVAR and BMT.However, in the long run, a signicantly lower incidence of adverse events was found in the TEVAR group compared to BMT, which included aortic rupture (OR 0.26), reinter­vention (OR 0.45), aortic-related death (OR 0.27) and all-cause mortality (OR
0.52). In addition, complete thrombosis of the thoracic false lumen and aortic
regression were signicantly more pronounced (better aortic remodelling). The message was that TEVAR is not superior to BMT in the short term, but should be implemented to improve long-term prognosis. The authors explained the different results compared to Hossack etal. [6] with the larger case numbers of the studies they included and the exclusion of complicated TBAD.
3.2.2 TEVAR inUncomplicated andComplicated TBAD
In a meta-analysis, Howard etal. [8] compared TEVAR in uncomplicated (n=8352) and complicated (n=7772) TBAD.Acute dissection was more frequent in the com­plicated TBAD group (73.55% vs. 66.91%), while chronic dissection was more common in uncomplicated TBAD patients (33.8% vs. 70.73%). Post-procedure
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