Surgical and endovascular management of acute type B aortic dissection

INTRODUCTION — The incidence of acute aortic dissection is estimated to be 5 to 30 cases per million population [1]. Type B aortic dissections are those that originate in the descending thoracic and/or abdominal aorta (distal to the left subclavian artery) (figure 1 and figure 2). For the purposes of our discussion, we use the term "acute" type B aortic dissection to refer to the period ≤90 days encompassing the hyperacute (<24 hours), acute (1 to 14 days), and subacute (15 to 90 days) periods as defined by the Society for Vascular Surgery/Society for Thoracic Surgery reporting guidelines that classify aortic dissection based on the timing from the onset of symptoms [2].

The primary treatment of uncomplicated acute type B aortic dissection remains medical [3,4], derived from the early experience in the 1960s that suggested better outcomes with medical management compared with surgery [5,6]. The goals of initial medical treatment of uncomplicated type B dissection are to stabilize the hemodynamics to minimize the extent of the dissection, reduce intimal flap mobility, and decrease the risk of rupture. For patients with uncomplicated acute type B dissection, mortality is low at 1 to 2 percent with medical therapy [7]. Untreated, 75 percent of all aortic dissection patients will succumb to their aortic dissection within the first two weeks [8]. (See "Management of acute type B aortic dissection", section on 'Anti-impulse therapy' and "Overview of acute aortic dissection and other acute aortic syndromes", section on 'Acute medical management' and "Management of acute type A aortic dissection", section on 'Acute management'.)

For patients who develop complications, intervention is indicated (endovascular, surgical). Patients with acute type B aortic dissection benefit from multidisciplinary management including expertise from cardiologists, vascular surgeons, cardiac surgeons, and interventional radiologists. For patients whose course is refractory to medical therapy, referral to a center with established expertise in aortopathies should be considered [9].

In spite of adequate medical management and surgical treatment, early mortality from acute type B aortic dissection remains significant, ranging from 10 to 15 percent, and contributes significantly to the overall mortality [10-13]. Since rupture is uncommon, occurring in fewer than 5 percent of all acute type B dissections, the majority of poor early outcomes are related to malperfusion [7,14]. Long-term survival is also limited by morbidity and mortality related to aneurysmal degeneration, which occurs in up to 50 percent of patients with asymptomatic type B aortic dissection with sufficient long-term follow-up.

The endovascular and surgical management of acute type B aortic dissection is reviewed here. The classification, clinical features, diagnosis, and medical management of type B aortic dissection are reviewed separately. The management of chronic type B aortic dissection and type A aortic dissection are also reviewed separately. (See "Clinical features and diagnosis of acute aortic dissection" and "Management of acute type B aortic dissection" and "Surgical and endovascular management of acute type A aortic dissection" and "Management of chronic type B aortic dissection".)

ETIOLOGY AND PATHOPHYSIOLOGY — Aortic dissections can be broadly divided into those that are degenerative (eg, atherosclerosis, inflammation/infection) and those that are genetically mediated, whether syndromic (eg, Marfan, vascular Ehlers-Danlos, Loeys-Dietz, and Turner syndromes) or nonsyndromic (eg, familial, associated with bicuspid aortic valve). (See "Epidemiology, risk factors, pathogenesis, and natural history of thoracic aortic aneurysm and dissection", section on 'Etiology and risk factors'.)

The pathophysiology responsible for initiating and propagating aortic dissection, leading to symptoms and signs, and the complications of type B aortic dissection are reviewed separately. (See "Clinical features and diagnosis of acute aortic dissection", section on 'Pathophysiology'.)

INDICATIONS FOR INTERVENTION — Intervention is indicated for patients with acute type B aortic dissection associated with complications [15], which typically occur within the first two weeks of diagnosis, affecting approximately 25 percent of patients with acute dissection [3,4,16,17]. This includes the following:

●Evidence of end-organ malperfusion (see 'End-organ malperfusion' below)

●Refractory pain in spite of adequate medical treatment (see 'Refractory pain in spite of adequate medical treatment' below)

●A rapidly expanding false lumen, which may be appreciated over the first several months following an acute presentation (see 'Rapidly expanding false lumen' below)

●Impending or frank rupture (see 'Impending or frank rupture' below)

End-organ malperfusion — Acute type B aortic dissection can be complicated by malperfusion syndromes, which occur because of false lumen propagation distally to occlude the thoracic or abdominal aortic branches. Branch occlusion can result in visceral ischemia (renal, intestinal, hepatic, splenic), spinal cord ischemia, or extremity ischemia [18,19]. The renal and mesenteric vessels are the most affected aortic branches. (See "Clinical features and diagnosis of acute aortic dissection", section on 'Symptoms and signs'.)

The time course of malperfusion is highly variable. Malperfusion can be present on initial presentation or develop anytime later; thus, any change in the patient's clinical condition should not be dismissed, particularly any aortic dissection involving the abdominal aorta or iliac vessels. Malperfusion that occurs after the acute dissection timeframe (ie, after two weeks) is uncommon but can imply a new dissection process, particularly if associated with acute pain [20]. (See 'Refractory pain in spite of adequate medical treatment' below.)

Malperfusion is typically manifested as clinical symptoms and signs in combination with laboratory markers and often confirmed with diagnostic imaging. Intestinal ischemia, spinal ischemia, and lower extremity ischemia are generally readily suspected based upon typical clinical features (eg, abdominal pain, paraplegia/paraparesis, pulse deficit). The clinical features and diagnosis of intestinal and lower extremity ischemia are reviewed elsewhere. (See "Overview of intestinal ischemia in adults" and "Acute mesenteric arterial occlusion" and "Clinical features and diagnosis of acute lower extremity ischemia".)

Renal dysfunction associated with renal artery obstruction due to acute type B aortic dissection is notoriously insidious in onset and often requires additional diagnostic evaluation to identify. Unilateral renal malperfusion can lead to resistant hypertension while bilateral malperfusion causes progressive renal insufficiency. Since hypertension is nearly universal in patients with acute type B dissection (both by history as well as at presentation), renal ischemia should be suspected based upon the evolution of marked difficulty in controlling hypertension, a rising creatinine, declining hourly urine output, or less commonly with flank pain. Any of these should prompt further diagnostic evaluation for renal malperfusion syndrome. (See "Renal infarction".)

Refractory pain in spite of adequate medical treatment — Although refractory pain was not associated with worse outcomes among patients with acute type B dissection in the absence of classic complications (ie, malperfusion) in one early study [20], in a later International Registry of Acute Aortic Dissections (IRAD) review that included 365 patients, a multivariable logistic regression model found that recurrent and/or refractory pain or refractory hypertension were significant predictors of in-hospital mortality (odds ratio 3.3, 95% CI 1.04-10.45) [21]. Refractory pain compared with no persistent pain increased the risk for in-hospital death overall (17.4 versus 4.0 percent), particularly among those only treated medically (35.6 versus 1.5 percent).

Rapidly expanding false lumen — Rapid expansion of the false lumen may be appreciated in early follow-up (zero to three months) computed tomography obtained in patients with acute type B aortic dissection. Rapid expansion is defined as >5 mm expansion of the total aortic diameter in six months, or >1 cm of expansion over one year. The significance of the acute expansion of the aorta immediately after aortic dissection (first weeks to month) is not known and may stabilize.

Impending or frank rupture — Increasing periaortic hematoma and hemorrhagic pleural effusion on imaging identify patients with complicated acute type B aortic dissection requiring urgent aortic repair [22,23]. However, rupture is uncommon, occurring in fewer than 5 percent of all type B dissections. (See "Clinical features and diagnosis of acute aortic dissection", section on 'Cardiovascular imaging'.)

Uncomplicated dissection at high risk for complications — Some clinicians have suggested that endovascular intervention may improve long-term outcomes in patients with uncomplicated acute dissection by favorably influencing the relationships of the true and false lumen and obliterating anatomy that would otherwise contribute to late morbidity and mortality [24-27]. Data supporting endovascular repair of patients with uncomplicated aortic dissection are in evolution, but a firm benefit for preemptive intervention has not been proven. Later-generation device technology may favorably influence the operative risk in the setting of acute dissection.

Findings associated with a high risk for the development of complications from the 2022 American College of Cardiology/American Heart Association (ACC/AHA) Guideline for the Diagnosis and Management of Aortic Disease includes [15]:

●High-risk imaging findings:

•Maximal aortic diameter >4 cm

•False-lumen diameter >2 to 2.2 cm

•Entry tear >1 cm

•Entry tear on lesser curvature

•Increase in total aortic diameter of >0.5 cm between serial imaging studies

•Bloody pleural effusion

•Imaging-only evidence of malperfusion

●High-risk clinical findings:

•Refractory hypertension despite more than three different classes of antihypertensive medications at maximal recommended or tolerated doses

•Refractory pain persisting >12 hours despite maximal recommended or tolerated doses

•Need for readmission

APPROACH TO REPAIR

Degenerative thoracic dissection — There is growing consensus that an endovascular approach may be preferred compared with an open surgical approach for treating complicated acute type B aortic dissection that has a sporadic (degenerative) etiology (ie, not associated with any genetically mediated syndromes), but data are limited to retrospective reviews [15,28-35]; there are no trials directly comparing endovascular with open surgery. This paradigm shift is due to a desire to reduce the appreciable morbidity and mortality associated with open surgical repair but acknowledges the limitations of contemporary endovascular procedures (endograft, fenestration), which may not reliably relieve obstruction of more distal aortic branches. (See 'Open surgery' below.)

Perioperative morbidity and mortality with open surgery for the treatment of acute, complicated type B aortic dissection has been high, with reported perioperative mortality rates that range widely from 20 to 50 percent [36,37]. Later data from the International Registry of Acute Aortic Dissection (IRAD) database suggest an improving mortality rate for complicated acute type B dissection with perioperative mortality rates of 17 percent with open surgery [10,37-44]. Invariably, these seemingly suboptimal outcomes are largely related to the presentation of the patient. In the IRAD study, hypotension/shock at presentation and periaortic hematoma were the primary determinants of mortality and poor outcome (60 percent mortality); those patients with normal blood pressure had fewer adverse outcomes [37]. Surgical therapy was most often graft replacement of the descending thoracic aorta (>80 percent of patients), and the repair technique included hypothermic circulatory arrest in nearly one half of the operations. The remainder of patients were treated with surgical fenestration [37].

In the first use of a stent-graft for patients with acute aortic dissection, 15 of 19 patients had complicated type B dissection (the others were type A dissections) [45]. Malperfusion in 22 vessels in 11 individuals was obstructed exclusively by dynamic mechanism, and all were reperfused by stent-graft placement alone. For those obstructed by a combination of dynamic and static mechanisms (15 vessels), 6 of the 15 reperfused after proximal stent-graft placement covering the entry tear. The technical success for eliminating false lumen flow was 100 percent. Later reports have similar initial technical success rates of 85 to 100 percent [46,47]. Overall mortality was 16 percent.

Early data from the IRAD registry suggested significant differences for in-hospital death depending upon the type of treatment. For surgically treated patients, mortality was 32 percent compared with 7 percent for those managed with endovascular techniques and 10 percent for those managed with medical therapy alone [10,13]. A systematic review identified five observational studies that included 318 patients [48]. Compared with surgery, the pooled perioperative mortality rate (four studies) was significantly reduced for endovascular compared with open repair (odds ratio 0.19, 95% CI 0.09-0.39). There were no significant differences between the groups for any of seven short-term complications, reintervention, or for long-term mortality. In a later IRAD review, perioperative mortality was significantly lower for endovascular repair compared with open surgery (11 versus 33 percent) [16]. Complications during hospitalization were also lower for the endovascular group (20 versus 40 percent). In a review of 3092 type B aortic dissections (acute, subacute, chronic), one- and two-year survival rates ranged from 80 to 90 percent, and 72 to 90 percent, respectively, which were improved compared with historical series of open surgical repair [26].

Genetic predisposition

Syndromic disorders — An open surgical approach to repair should be used in patients with syndromic thoracic aortic aneurysm/dissection (TAAD; eg, Marfan (table 1), vascular Ehlers-Danlos, Loeys-Dietz, and Turner syndromes) [15]. Aortic stent-grafts should not be used in the native thoracic or abdominal aorta in these patients. Marfan syndrome and other connective tissue disorders have been a strict exclusion criterion in all commercial stent-graft trials. The reliability of deployment of a stent-graft in the fragile milieu of the Marfan aorta and the question of what effect the persistent radial force of the stent-graft may have on the Marfan aorta remain unanswered questions.

An expert consensus recommended against endovascular repair for these patients unless the risk of open surgery is deemed truly prohibitive at a center experienced in management of complex aortic disease [49]. This opinion is shared by most surgeons experienced in central aortic surgery. A report of thoracic endovascular repair in eight patients with connective tissue disorder (six with Marfan syndrome, two with vascular Ehlers-Danlos syndrome) demonstrated initial success with few major complications, but a high rate of secondary intervention was needed due to continued aortic expansion [50]. These authors and others have proposed that the technique may be justified in emergencies as a "bridge" to stabilize ruptured and critically ill complicated dissections, allowing transfer after initial TEVAR [50,51]. No long-term follow-up was provided in the study, but in another report [52], Marfan syndrome was an independent predictor of late aneurysm. Another study recommended endovascular repair only in instances of late localized pseudoaneurysm with stenting over native tissue from "graft to graft" [53].

Nonsyndromic disorders — The approach to repair of acute type B dissection in patients with nonsyndromic disorders, most commonly familial thoracic aortic aneurysm/dissection (TAAD), is less certain. Because family history and assignment of unexpected deaths may lead to over assignment or attribution to aortic catastrophe, evaluation by a genetic counselor may be useful in decision making for young patients. The age at presentation for patients with familial type B dissection is younger compared with type A dissection or sporadic type B dissection, which may favor an open approach. In one review of 70 patients with familial TAAD (specifically ACTA2 mutations) presenting with aortic events, 10 had an acute type B dissection [54]. Six of the acute type B dissections required repair: two were repaired with open descending aortic replacement, one with aortobifemoral bypass, and three with endovascular repair.

Isolated abdominal aortic dissection — Isolated abdominal aortic dissection is an uncommon variant of a type B dissection. The incidence in one IRAD study was 1.3 percent (18 of 1417 patients enrolled) [55]. A presentation that included abdominal pain, mesenteric infarction, or limb ischemia was more prevalent in isolated abdominal aortic dissection compared with a typical dissection emanating from a tear near the left subclavian artery. Hypotension was present in 12 percent, which was a greater incidence compared with typical type B dissection, and thus the presentation is not likely to be easily distinguished from ruptured abdominal aortic aneurysm without imaging.

The outcome of medically treated patients with isolated abdominal aortic dissection is worse compared with that of patients with typical type B dissection. In the IRAD study, 33 percent of patients treated medically had died at four-year follow-up, compared with none of the patients treated with open surgery or endovascular repair. In light of this late mortality exceeding typical type B dissection, early repair may be justified. Given the complicated anatomy, most abdominal aortic dissections are not amenable to endovascular repair and will require an open approach, although an endovascular approach has been described [56,57].

ENDOVASCULAR REPAIR — Several types of endovascular interventions can be used in the management of acute type B aortic dissection. Endovascular interventions for acute type B aortic dissection are complementary, and a given patient may require any one procedure, or combination of procedures, to reliably relieve malperfusion. As a secondary goal, though not yet proven, endovascular stent-graft therapy may reduce the incidence of late aneurysmal degeneration by reducing false lumen flow. For patients with aortic rupture, endovascular repair is feasible but may require adjunctive embolization of the false lumen to stop ongoing bleeding [58]. Endovascular techniques have also been used to manage immediate or delayed complications related to primary endovascular repair (eg, endoleak, stent migration) or late chronic issues (eg, late aneurysmal dilation) related to medically or surgically treated type B aortic dissection [59,60]. (See 'Indications for intervention' above and "Management of chronic type B aortic dissection", section on 'Endovascular repair'.)

The following endovascular techniques are used to manage type B dissection complicated by malperfusion. As experience with endovascular coverage of the proximal entry tear has occurred, fenestration and stenting of branch vessels have become adjuncts to stent-grafting rather than definitive therapy. (See 'Techniques' below.)

●Stent-graft coverage of the primary tear in the proximal descending thoracic aorta to obliterate false lumen flow and increase true lumen perfusion (figure 3). One to two centimeters of undissected aorta must be present to provide stent fixation.

●Assessment of aortic branches for patency and stenting if residual branch dissection or stenosis is identified.

●Consideration for balloon fenestration of the dissection septum if proximal entry tear coverage is not technically feasible or not effective.

Devices used for endovascular thoracic aortic repair are discussed separately. (See "Endovascular devices for thoracic aortic repair".)

Vascular imaging — Arteriography is more important for the assessment of the distal branch vessel anatomy and the determination of the need for branch vessel stenting. Powered injections should be avoided, particularly into the true lumen of the dissected aorta, because they can falsely reduce the flap mobility and produce an apparent dynamic aortic obstruction that may or may not exist.

The initial technical approach for an endovascular intervention in acute type aortic dissection relies heavily upon intravascular ultrasound. Ultrasound can document the location of the proximal entry tear, the anatomy of visceral and renal branches in relation to the true and false lumens and can identify the dissection septum that may be overlying branch orifices to produce malperfusion in a dynamic or static manner. For patients with iliofemoral thrombosis or leg malperfusion, ultrasound also identifies the compressed true lumen and can aid with needle and wire introduction.

Techniques

Coverage of entry tear — Coverage of the entry tear with a stent-graft restores perfusion in approximately 75 percent of patients by relieving dynamic aortic obstruction [45-47]. (See "Clinical features and diagnosis of acute aortic dissection", section on 'Pathophysiology'.)

The technique for aortic stent-graft placement for patients with aortic dissection has several important differences compared with thoracic endovascular aortic repair (TEVAR) for thoracic aneurysm. (See "Endovascular repair of the thoracic aorta".)

Although secure proximal fixation is needed for both pathologies, patients with aortic dissection very commonly have little to no distance from the left subclavian artery origin to the intimal tear. Thus, coverage of the left subclavian artery may be required more often. This is usually well tolerated without significant arm symptoms. The optimal extent of coverage of the thoracic aorta and deployment of stent-grafts remains unclear. It is likely that a longer stent-grafted length may be more effective for achieving thrombosis of the false lumen, but this may be at the expense of an increased risk for paraplegia.

Stabilization of distal flap — The PETTICOAT (provisional extension to induce complete attachment) technique uses a proximal endograft and distal bare metal stent. The distal bare metal stent is placed into the aortic true lumen, distal to the proximal endograft, and aims to stabilize the distal collapsed intimal flap, while allowing blood flow to visceral arteries [61]. In studies evaluating the safety and efficacy of a composite device design (covered stent-graft plus bare metal stent; ie, dissection stent), the dissection stent was used in 58 of 73 patients [29,62]. At the 12-month follow-up, complete or partial thrombosis of the false lumen was seen in 100 percent of patients within the stent-graft region and in 97.4 percent of patients within the dissection stent region. Expansion >5 mm of the maximum transaortic diameter was observed in 14.9 percent of patients in the stent-graft region and in 38.5 percent of patients within the dissection stent region.

Stenting visceral branch obstruction — Additional stenting of persistent dynamic obstruction or static obstruction of the distal branch vessels may be required in many patients. Malperfusion of the aortic branches is defined during the procedure as a systolic gradient of >10 mmHg from the aorta into the distal branch.

To rectify these gradients, a self-expanding stent can be used to reduce flap mobility within the branch lumen. Balloon-expandable stents into the proximal visceral, renal, and iliac vessels should be avoided as they may be crushed by the dissection flap mobility. (See "Surgical and endovascular techniques for mesenteric revascularization" and "Renal artery aneurysm".)

The technical success of branch vessel stenting to reduce gradients can approach 90 percent, and complications related to stenting are rare (<10 percent) [63]. Most complications relate to minor access site complications (eg, bruising, bleeding, hematoma).

Fenestration of septum — Fenestration of the intimal flap (ie, creating a communication between the true and false lumen) may be performed with one of several techniques that use a combination of ultrasound and fluoroscopy for guidance [64]. The ideal hemodynamic result for fenestration of the dissected intima is equalization of peak systolic pressures between the two lumens in the aorta, and decompression of the false lumen. However, because of the potential dramatic and unpredictable alterations in intimal flap anatomy and flow dynamics that can occur by overly aggressive fenestration in the visceral aorta, investigators with the largest series of patients recommend limiting percutaneous fenestration to the distal thoracic and abdominal aorta [65].

In a series of 40 patients with malperfusion syndromes, 14 patients underwent combined stenting and balloon fenestration, 24 underwent stenting alone, and 2 underwent fenestration alone [65]. The location of the balloon fenestration was in the thoracic aorta in eight patients, in the upper abdominal aorta in three patients, and just above the aortic bifurcation in seven patients. Flow was restored to the ischemic territories in 37 of 40 patients (93 percent), but the 30-day survival was 75 percent. After the periprocedural period, five additional patients died, with one of these deaths related to false lumen rupture and two of unknown etiology. This perioperative mortality rate of 25 percent compares favorably with the historical surgical series for open surgical fenestration.

The effect of fenestration on long-term outcomes with respect to false lumen expansion in patients with distal dissections is unknown, since the false lumen remains pressurized and therefore at risk for continued progression to aneurysm. In one series of 46 patients with malperfusion treated by either stent-graft therapy (n = 12) or balloon fenestration (n = 34), the aortic diameter decreased in patients treated with stent-grafts but increased in those with balloon fenestration only [66].

Techniques for fenestration include the following:

●Fenestration is most often performed from the smaller (usually true lumen) to the larger false lumen. A fenestration (hole, new opening) is created near the compromised aortic branch using a Rösch-Uchida needle, Brockenbrough needle, Colopinto needle, or the back end of a 0.014 wire. After the needle and a stiff wire are advanced from the true to the false lumen, a 5 F catheter is advanced. Confirmation of the position across the membrane is performed by contrast injection. Subsequently, an angioplasty balloon of at least 12 to 15 mm in diameter and 20 to 40 mm in length is used to create a fenestration tear.

●An alternative technique of fenestration has been termed the "scissors technique" [67]. Stiff guidewires are placed in each lumen from a single femoral access, and a single long sheath is advanced over the two wires, thus dividing the membrane over this distance. Those familiar with the use of the "scissors technique" have reported both clean longitudinal tears (the ideal result) and circumferential separation of the flap from the aortic wall with aorto-aortic intussusception (not ideal) [68].

●Another technique uses a snare that can be used to deliver a wire from one femoral access through the flap and down the contralateral femoral access. By pulling this upside-down "U" toward the distal aorta, a fenestration defect may be created, but this technique has the same potential risk of intimal dehiscence.

Complications of endovascular repair — In general, complications related to endovascular access and aortic stent-grafting are like endovascular repair for other indications (eg, abdominal aortic aneurysm) and include stroke, paraplegia, renal failure, and death. Major complications occur in 40 to 80 percent of patients [46,47]. Paraplegia rates are generally low, ranging from 0 to 3 percent [18,25,29,47,58,66,69], although one study reported a rate of 13.5 percent [47]. These rates are similar to reported rates for endovascular repair of other pathologies (eg, thoracic aortic aneurysm, blunt aortic injury). (See "Endovascular repair of the thoracic aorta", section on 'Ischemic complications'.)

Reintervention rates ranged from 19 to 33 percent and increased with longer follow-up [69,70]. In one study, 14 of 41 patients required reintervention for stent-graft migration, endoleak, aneurysmal expansion, and retrograde dissection [59]. On univariate analysis, false lumen thrombosis was associated with a lower risk for reintervention. Technical complications immediately related to stent-graft placement are unusual but may be lethal and unanticipated. One such procedural complication is retrograde dissection into the ascending aorta, which can occur immediately during device placement or later during follow-up [71]. The incidence is approximately 1 to 2 percent during the procedure and 1 to 20 percent with longer follow-up [72,73]. Delayed presentations with acute chest pain, syncope, or sudden death can occur any time after device placement. Outcomes of the event are often lethal, with mortality rates up to 40 percent for retrograde type A dissection, regardless of treatment [73]. (See "Surgical and endovascular management of acute type A aortic dissection".)

Apart from secondary intervention for retrograde dissection, secondary device-related interventions may be required to obliterate flow in the false lumen. At one year after stent-graft placement for acute type B dissection, thrombosis of the false lumen adjacent to the device occurs in 70 to 80 percent of patients [74,75]. A much lower rate of false lumen thrombosis occurs after stent-grafting for chronic dissection [76]. Most chronic false lumens remain patent via abdominal aorta reentry tears of the dissection septum in proximity to the origins of the visceral and renal vessels. It is not technically feasible to obliterate these with current technology.

OPEN SURGERY — Replacement of the proximal descending thoracic aorta and surgical fenestration are the main surgical options for managing acute type B aortic dissection. An open surgical approach replacing the thoracic aorta to the extent needed is recommended for patients with genetically mediated type B aortic dissection, rather than endovascular stent-graft placement [4]. (See 'Genetic predisposition' above.)

Impending or frank rupture of the aorta is most often addressed by open surgical graft replacement of the descending thoracic aorta. Surgical fenestration is reserved for malperfusion that cannot be resolved rapidly by endovascular means. When there is iliac artery thrombosis, aortofemoral bypass grafting can be performed by sewing a graft to the infrarenal aorta and bringing the limbs into the groin to sew onto the femoral arteries.

Thoracic aortic grafting — Replacement of the thoracic aorta for aortic dissection is similar to thoracic aortic replacement for other indications. (See "Overview of open surgical repair of the thoracic aorta".)

Abdominal aortic fenestration/grafting — Surgical fenestration involves wide resection of the septum of the dissection, which is creating the dynamic aortic branch obstruction, but is rarely needed given that proximal stent-graft therapy to cover the thoracic aortic entry tear suffices in many patients. The visceral and renal segment of the aorta may be considered for surgical fenestration when proximal stent-grafting and branch vessel stenting fail to control dynamic aortic obstruction. The procedure can be performed through a 9^th or 10^th intercostal space incision extending onto the anterior abdominal wall. The peritoneal contents can also be inspected for viability through the exposure. The distal thoracic aorta is cross-clamped and the aorta opened along its longitudinal axis, and the dissection flap in the upper abdominal aorta is resected.

Advocates for surgical fenestration assert that the results of treatment of acute type B dissection are often related to delays in diagnosis and treatment. The available literature would support such a notion, but it is limited by the low number of patients available for comparison. In a series of seven patients with ongoing renal and lower extremity ischemia treated with visceral aorta fenestration, no patients died, and temporary dialysis was required in only two cases [77]. By comparison, in another series of 14 patients treated with surgical fenestration, mortality was 43 percent with all those who died noted to have a >48 hour delay from the time of the diagnosis of malperfusion to fenestration [78]. Long-term performance of surgical fenestration for acute type B dissection has been reviewed [58,79-82]. In one study, the actuarial survival of the patients undergoing fenestration (n = 14) was 77 percent at one year and 53 percent at five years. The chief indication for fenestration was lower extremity ischemia, and infrarenal fenestration and aortobifemoral grafting were the procedures used. None of the late deaths was related to aortic disease, and none of the fenestrated aortas developed aneurysmal degeneration during follow-up [79].

Surgical fenestration may also be a viable option in patients who present with type A dissection and undergo standard ascending aorta repair but have evidence of ongoing malperfusion. In these patients, the presence of the residual aortic dissection in the arch may not allow secure stent-graft deployment and fixation to divert blood flow from the false lumen. As such, a direct surgical fenestration may provide definitive therapy if there is malperfusion of multiple territories (renal, visceral, lower extremity).

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Aortic dissection and other acute aortic syndromes".)

SUMMARY AND RECOMMENDATIONS

●Type B aortic dissection – Type B aortic dissections are those that originate in the descending thoracic and/or abdominal aorta (distal to the left subclavian artery) (figure 1 and figure 2). Patients with acute type B aortic dissection benefit from multidisciplinary management including expertise from cardiologists, vascular surgeons, cardiac surgeons, and interventional radiologists. For patients whose course is refractory to medical therapy, referral to a center with established expertise in aortopathies should be considered. (See 'Introduction' above.)

●Uncomplicated type B aortic dissection – The primary treatment of uncomplicated acute type B aortic dissection (figure 1) is anti-impulse therapy consisting of heart rate and blood pressure control to minimize the extent of the dissection, reduce intimal flap mobility, and decrease the risk of aortic rupture. (See "Management of acute type B aortic dissection", section on 'Anti-impulse therapy' and "Overview of acute aortic dissection and other acute aortic syndromes", section on 'Acute medical management'.)

•For patients with uncomplicated acute type B aortic dissection who do not meet any of the criteria listed below for complicated type B aortic dissection, ongoing conservative medical management is recommended rather than any form of intervention (endovascular or surgical). For medically treated patients who do not develop complications, mortality is low at 1 to 2 percent.

•However, there may be a potential long-term benefit for preemptive endovascular intervention, but this has not yet been proven. Imaging and clinical findings associated with a high risk for developing complications include the following:

-Maximal aortic diameter >4 cm

-False-lumen diameter >2 to 2.2 cm

-Entry tear >1 cm

-Entry tear on lesser curvature

-Increase in total aortic diameter of >0.5 cm between serial imaging studies

-Bloody pleural effusion

-Imaging-only evidence of malperfusion

-Refractory hypertension despite more than three different classes of antihypertensive medications at maximal recommended or tolerated doses

-Refractory pain persisting >12 hours despite maximal recommended or tolerated doses

-Need for readmission

●Complicated type B aortic dissection – Patients with complicated type B aortic dissection undergo repair. Criteria for include (see 'Indications for intervention' above):

•End-organ malperfusion (eg, end-organ ischemia, refractory hypertension)

•Refractory pain in spite of adequate medical treatment

•Rapidly expanding false lumen, active bleeding, impending rupture, or frank aortic rupture

•Aneurysmal dilation in a region of aortic dissection

●Malperfusion syndromes – Malperfusion syndromes occur because of distal propagation of the false lumen that occludes one or more thoracic or abdominal aortic branches, leading to renal ischemia, visceral ischemia (intestinal, hepatic, splenic), extremity ischemia, or spinal cord ischemia. The most affected aortic branches are the renal and mesenteric vessels. The time course of malperfusion is highly variable, and frequent clinical assessment is important. However, malperfusion that occurs after the acute dissection timeframe (>2 weeks) is uncommon and can imply a new dissection process, particularly if associated with acute pain. (See 'End-organ malperfusion' above.)

●Intervention

•Repair of degenerative thoracic aortic dissection – For most patients with sporadic (degenerative) acute type B thoracic aortic dissection (ie, not associated with any genetically mediated syndromes) with malperfusion and meeting anatomic suitability for endovascular repair, we suggest endovascular stent-grafting to cover the primary entry tear in the proximal descending thoracic aorta, rather than open surgical repair or fenestration or another type of endovascular intervention (Grade 2C). Perioperative mortality is significantly improved for endovascular compared with open repair, but the overall complication rates and long-term survival rates are similar. An open surgical approach may be necessary to manage patients with rupture to rapidly control hemorrhage. (See 'Degenerative thoracic dissection' above and 'Endovascular repair' above.)

•Repair of genetically mediated thoracic aortic dissection – For patients with genetically mediated (syndromic or nonsyndromic) acute thoracic aortic dissection (eg, Marfan, vascular Ehlers-Danlos, Loeys-Dietz, familial) as an etiology for acute type B aortic dissection and any indication for intervention, we suggest an open surgical approach to replace the descending thoracic aorta to the extent needed, rather than endovascular stent-grafting (Grade 2C). This subpopulation has been excluded from most trials comparing endovascular with open surgery. Among those in whom endovascular stent-grafting has been tried, unfavorable late aortic remodeling at the site of stent-graft placement is seen related to the persistent radial force of these devices. However, some feel that stent-grafting may be justified in emergency settings as a "bridging" method to later definitive surgical repair. (See 'Syndromic disorders' above.)

•Managing persistent malperfusion – For patients who have ongoing obstruction of one or more distal aortic branches despite proximal thoracic aortic endovascular stent-graft deployment, adjunctive endovascular techniques such as endovascular balloon fenestration or aortic branch stent placement may help resolve malperfusion. Surgical fenestration is uncommonly needed but may be necessary, particularly among those with persistent lower extremity malperfusion (typically combined with aortofemoral grafting). (See 'Fenestration of septum' above and 'Stenting visceral branch obstruction' above and 'Abdominal aortic fenestration/grafting' above.)