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444
CH
35
F
E
FIGURE 358Cont'd E, Graft is
G
I
H
J
sutured to proximal descending thoracic aorta. F, Clamps are repositioned to restore perfusion of left subclavian artery, left heart bypass is stopped, and remainder of aneurysm is opened. G, Dissecting membrane is removed to allow identification of patent segmental arteries and origins of visceral and renal arteries. H, Blood from left heart bypass circuit is delivered to celiac axis and superior mesenteric artery (SMA) via balloon perfusion catheters. Cold crystalloid is delivered to kidneys through catheters placed in renal arterial ostia. Critical intercostal arteries are attached to an opening in graft. I, Reattachment of visceral branches and (J) the distal aortic anastomosis complete the repair.
Box 35-4 Strategies for Spinal Cord, Visceral, and
Renal Protection During Repair of Distal Thoracic Aortic Dissection
All Extents
Permissive mild hypothermia (32°C-34°C, nasopharyngeal) Moderate heparinization Aggressive reattachment of segmental arteries (especially T8-L1) Sequential aortic clamping when possible Perfusion of renal arteries with 4°C crystalloid solution when possible
Extent I and II Thoracoabdominal Repairs
Cerebrospinal fluid drainage Left heart bypass during proximal anastomosis Selective perfusion of celiac axis and superior mesenteric artery (SMA)
during intercostal and visceral/renal anastomoses
OUTCOMES
When performed in specialized centers, these operations achieve excellent survival with acceptable morbidity. tality for chronic distal dissection repair ranges from 6% to 10%. Predictors of operative mortality include increasing age, congestive heart failure (CHF), aortic rupture (contained or free), and preopera­tive renal failure. Risk of paraplegia or paraparesis is 3% to 9%. These outcomes are significantly better than those obtained in patients who undergo surgery during the acute phase. For example, comparative
67,77,78,81,93–95
Early mor-
93
Postoperative Considerations
While preventing hypertensive episodes, maintaining adequate blood pressure, preload, and cardiac inotropic state are important in preventing delayed paraplegia and postoperative renal failure. In the absence of postoperative bleeding, blood pressure should be kept near its preoperative baseline level. Delayed paraplegia can arise hours to days after aortic surgery. In the postoperative period,
strategies to reverse paraplegia include inducing systemic hyper-
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tension, decreasing cerebrospinal pressure by cerebrospinal fluid drainage, correcting anemia, preventing fever, and administering cardiac inotropes, mannitol, and steroids.
96
Recovery from paraple­gia is possible, but if cord function does not return promptly after these measures are taken, such a recovery is not likely.
Aortic graft infections are a threat to anastomotic integrity and are associated with extremely high morbidity and mortality.97 Definitive treatment often requires complete removal of the graft and complex vascular reconstruction. In an attempt to prevent this complication, administration of IV antibiotics is recommended until all drains, chest tubes, and central venous lines are removed. Similarly, all post­operative infections are treated aggressively with parenteral antibiot­ics to minimize the risk of secondary graft infection.
Vocal cord paresis is not uncommon after dissection at the dis­tal arch. Resulting hoarseness is a concern that affects both voice and postoperative pulmonary toilet (owing to ineffective cough). Thyroplasty can improve functional status and is performed early before discharge.
98
An exception would be in the event of antici­pated reintubation for a planned subsequent operation, such as completion of an elephant trunk. Reintubation can potentially dis­turb the thyroplasty, in these cases, initial vocal fold medialization can be achieved via collagen injection, and definitive thyroplasty can be performed at a later time.
The View Ahead
The landscape of thoracic aortic surgery is changing rapidly. As patient age and disease complexity continue to increase, new challenges are being met with innovative treatment strategies and technological advances. As we gain experience with endovascu­lar aortic stent-grafts, new indications are being explored (see Chapter 36). The role of stent-grafts continues to expand in both the hybrid setting and stand-alone situations. Improvements in our understanding of the molecular mechanisms of dissection may lead to novel forms of medical treatment aimed at reducing the rate of aortic expansion and risk of fatal rupture.
Acknowledgments
The authors express gratitude to Chrissie Chambers, MA, ELS, and Stephen
N. Palmer, PhD, ELS, of the Texas Heart Institute, and Susan Y. Green, MPH, for editorial assistance; and Scott A. Weldon, MA, CMI, and Carol Lawson, CMI, for creating illustrations and assisting with image selection.
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SURGICAL THERAPY FOR AORTIC DISSECTION
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CHAPTER
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36 Endovascular Therapy for Aortic
Dissection
Michael D. Dake
Acute aortic dissection (AAD) is a precipitous event associated with a wide range of outcomes from uncomplicated to cata­strophic. Current endovascular strategies are based on identifying features that portend increased risk of death or other poor out­come and applying interventional techniques to prevent the life­threatening complications of the dissection.
During the last 2 decades, there has been increasing interest in exploring endovascular procedures for management of aortic dissection. addressing branch vessel involvement and ischemic complications associated with the dissection process endovascular aortic stent grafts (initially developed to repair aor­tic aneurysms) were applied in type B aortic dissection to cover the primary entry tear of the dissection and promote thrombosis of the thoracic aortic false lumen cular tactics are now routine in the contemporary armamentarium for treatment of aortic dissection and its myriad manifestations.
Endovascular approaches are complementary to the two tradi­tional therapeutic paradigms of open surgical repair for type A dis­section and medical treatment for uncomplicated type B disease. Invasive interventional procedures fit between the existing opera­tive and noninvasive alternatives to provide effective options for type A dissection with severe branch vessel compromise (before or after ascending aortic repair), complicated type B dissection (branch vessel involvement, descending aortic rupture, exten­sion of disease or early aortic dilation, etc.), arch involvement, and ascending aortic intramural hematoma associated with an intimal tear distal to the left subclavian artery.
This chapter will review the specific endovascular procedures currently in use to manage aortic dissection, the patient subgroups in which these techniques are commonly employed, and the outcomes of these interventions.
4–13
Initially, endovascular approaches focused on
4,5
(Fig. 36-2). These basic endovas-
1–3
8,9
(Fig. 36-1). Subsequently,
Branch Vessel Interventions
Branch vessel involvement accompanying aortic dissection is a well-recognized complication occurring in over 30% of
7,8,14
cases. tomical concepts of static and dynamic branch involvement are crucial to selection of the endovascular option for reperfusion of an affected vascular bed. distally from the primary entry tear, the dissection septum may engage the ostia of branch vessels. If the aortic flap, which con­sists of the intima and portion of the media shorn away from the wall, engages a branch orifice as it extends, two pathophysiologi­cal situations referred to respectively as static and dynamic branch involvement may occur (
Static Branch Involvement
One manifestation that may arise when the advancing dissection septum intersects an aortic branch is static branch vessel involve­ment ( extends directly into the branch for a variable distance. In contrast to the geometry described earlier, orientation of the septal trajec­tory is such that the branch ostium is incompletely engaged by the edge of the dissection plane. Rather than being circumferentially shorn by the septum, there is only partial circumferential involve­ment of the branch by the dissection. The aortic flap extends into the branch, creating a false lumen within the artery. As a result, the individual branch has both a true and false lumen like the aorta.
For appropriate intervention selection, the pathoana-
15–17
As the dissection process extends
Fig. 36-3).
Fig. 36-4). In static involvement, the aortic dissection flap
Similar to the aorta, a branch affected by static involvement may have multiple fates. At the end of the dissection where the flap ter­minates in the branch, a reentry tear in the false lumen may or may not occur. If a reentry tear occurs at the end of the false lumen, branch perfusion results from blood flow in both the true and false lumens. In many such cases, dual lumen perfusion is not associ­ated with ischemic branch vessel symptoms. If reentry does not occur in cases of static branch vessel involvement, however, the false lumen within the branch has no outflow. The absence of a distal tear to allow communication with the vascular bed beyond the dissection may impair blood flow significantly. This no reen- try state within the branch's false lumen renders perfusion lim­ited to that contributed by the true lumen. Unfortunately, the true lumen may be compromised by the engorged false lumen. The blind pouch of the false lumen, without outflow, swells to a maxi­mum dimension at its distal end. The pressure exerted by the false lumen severely distorts and compresses the true lumen to mark­edly reduce branch vessel flow. Commonly, the degree of ischemia experienced by the involved vascular bed may be significant and can lead to irreversible tissue necrosis if not relieved quickly.
In no-reentry situations, a local solution directed at improving flow within the affected artery is required because the problem is localized within the specific branch. Two options for endovascu­lar treatment are possible. Resistance to outflow within the false lumen may be decreased by creating a distal tear or fenestration within the blind channel. This can be accomplished with the end of a guidewire or other endovascular probe placed within the false lumen through the aortic false lumen. This approach is associ­ated with practical challenges, including the avoidance of distal extension of the dissection process, safe penetration of the false lumen wall to create an effective outflow tear, and determination of the presence of thrombus within the blind sac of stagnant false lumen blood to avoid its distal embolization.
In most cases, the preferred strategy involves increasing branch flow by decreasing the resistance to true lumen blood flow. This is performed by placing a stent in the true lumen of the branch through catheterization from the aortic true lumen. The stent is typ­ically placed from beyond the end of the false lumen in the branch back to the aortic true lumen. A self-expanding nitinol stent is commonly employed because this distance is frequently greater than 2 cm and because there is a risk of squeezing any existing clot out of the false lumen with a balloon-expandable stent. These stents are sized to the total transarterial diameter of the branch and allowed to progressively expand on their own (post deployment) without supplemental balloon dilation. There are many success­ful reports of this approach in mesenteric, renal, and iliac arteries affected by no-reentry or static involvement.
Occasionally, static branch vessel involvement with reentry anatomy and double-barrel flow may require endovascular inter­vention. The most common indication for stent placement in this setting occurs with involvement of a renal artery ( kidney supplied by a dissected renal artery may be affected by the physical presence of a flap within the branch. The variable flow reduction caused by the flap, and resultant disrupted pattern of true and false lumen perfusion, may contribute to an exacerbation of hypertension. In cases where high blood pressure is sustained and recalcitrant to numerous intravenous ( IV) medications, endo­vascular intervention may be warranted to restore a single lumen without flap. The approach to treatment involves placement of a balloon-expandable renal stent within the true lumen of the renal artery through the aortic true lumen. In most cases, this type of
8,9,18,19
Fig. 36-5). The
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A B
FIGURE 361 Type B aortic dissection with proximal entry tear distal to left subclavian artery, retrograde extension, ascending intramural hematoma, and rupture into left chest. A, Non–contrast-enhanced axial computed tomography (CT) image through the aorta demonstrates an ascending aortic
mural-based ring with increased density, indicative of intramural hematoma. Also apparent is abnormal extravascular tissue surrounding aorta, with characteristic appearance of a rupture with clot. B, Series of images from a thoracic aortogram demonstrate entry tear just beyond left subclavian artery, with contrast media opacifying both the true and false lumens. Precise point of rupture is not identified.
A B
FIGURE 362 Aortic dissection with rupture. A, Thoracic aortogram demonstrates type B aortic dissection with mid-descending aortic rupture. B, Repeat aortogram following placement of thoracic endograft over proximal entry tear just above the site of rupture, without evidence of residual contrast extravasation.
TL
FL
A
FIGURE 363 A, Static obstruction. Dissection has extended into a branch vessel. B, Dynamic obstruction. Membrane is lying across and obstructing origin of branch vessel. TL, true lumen; FL, false lumen.
B
FL
TL
ABC
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FIGURE 364 Magnetic resonance imaging (MRI) of static branch vessel involvement of iliac arteries. A, Coronal image of pelvis identifies a flap extending into right common iliac artery (CIA) and down to distal external iliac artery (EIA). Flow is evident in both true and false lumens within the right iliac artery. This is an example of static involvement with direct flap extension from the aorta into a branch. At the end of the dissection within the EIA, there is a distal reentry tear. This terminal tear establishes double-barrel flow within the iliac artery, which is rarely associated with ischemic symptoms. B-C, Similar coronal views show flap extension into left iliac system, but a segmental flow void (black segment) within false lumen of left CIA. This is associated with a no-reentry situation at distal extent of false lumen. No reentry within a branch is typically associated with obstruction of true lumen by a dilated false lumen cul-de-sac. The flow void noted may represent thrombosis in a blind channel or simply no blood flow. The usual consequence of this phenomenon of no reentry is branch vessel ischemia due to a lack of false lumen perfusion and compromised true lumen branch flow.
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Bilateral Renal Art cpr
A
FIGURE 365 Computed tomography (CT) images of true and false lumen relationships to renal arteries. Axial (A) and coronal (B) CT images at level of left renal artery show that left renal artery is supplied by the false lumen (left aortic lumen). True lumen is located along right wall of aorta, and flap shows a characteristic natural fenestration or defect corresponding to left renal ostium. Flap around fenestration has small tail-like extensions pointing to the left that represent the initial few millimeters of left renal intimal lining that were torn away with the retracted aortic septum.
reentry involvement does not extend into the branch as far as the no-reentry extension. Thus, stents less than 2-cm long are typically implanted. This technique is well established at most centers that manage cases of aortic dissection frequently.
B
distally. The cleavage plane extends 1 to 2 mm into the branch, and then circumferentially reenters, creating a cylindrical tear, coring out a short segment of the intimal/medial lining of the most proxi­mal aspect of the branch. The septum retracts into the aortic lumen with a fenestration corresponding to the branch orifice. This gives
Dynamic Branch Involvement
In addition to primary branch pathology that occurs as a com­plication of aortic dissection, another mechanism, dynamic branch vessel involvement, may be responsible for organ isch­emia. Dynamic branch involvement is a phenomenon associated with obstruction to branch vessel flow by an aortic septum that has prolapsed over the branch ostia like a curtain. In contrast to static involvement, where the aortic flap extends directly into a branch, dynamic obstruction occurs as an aortic process exclu­sively without an associated branch lesion. Propagation of the aor­tic flap may create a circumferential cleavage of the aortic wall surrounding the branch ostium (Fig. 36-6). Factors associated with this event include the flap trajectory, the resultant orientation of the septal plane proximal to the branch, and the inclusion of the ostium by the cleaved flap as it extends past. In this situation, the dissection septum surrounds the branch ostium as it tears
the flap a stencil-like appearance when viewed en face, with the number of holes related to the number of branch vessels involved by this phenomenon. When imaged in an axial plane, the affected artery appears to originate exclusively from the aortic false lumen. Closer inspection usually allows identification of a tear in the flap at the level or adjacent to the level of the branch. The flap often displays small projections angled from the edge of the tear, giving its outline on axial imaging an appearance similar to the contour of a metal rivet, the short-legged extensions corresponding to the amputated proximal lining of the branch.
In dynamic branch obstruction, hemodynamic flow patterns result in a large aortic false lumen with a diminutive or col­lapsed true lumen. There is variability, however, in the degree of true lumen obliteration related to the dynamic compromise.
In the majority of aortic dissection cases with true and false lumen aortic flow (often called double-barrel flow), the process described does not cause critical branch perfusion abnormalities.
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FIGURE 366 Magnetic resonance imaging (MRI) demonstrates dyna­mic branch vessel involvement, with aortic true lumen collapse and accompanying static no-reentry obstruction of left common iliac artery (CIA). A-C, Axial MRI shows
wafer-thin crescent-shaped true lumen collapsed against anterior aortic wall at level of visceral arteries. Aortic septum prolapses like a curtain across the origins of branches originating from true lumen, with resultant malperfusion and multiorgan ischemia. D, At the level just below aortic bifurcation, there is marked asymmetry in appearance of CIAs. Lumen of left CIA has a flow void (black circle) due to static involvement without reentry that coexists with the dynamic process observed more proximally.
Flow to the branch originates primarily from the false lumen, with a small contribution from the true lumen through the corresponding fenestration in the aortic septum. Most of the false lumen flow usu­ally occurs in diastole. During systole, the small contribution from the true lumen arrives through the septal window into the false lumen and branch. If the proximal primary tear is very large or the entry tear is in close proximity to the branch, the dominant flow pattern supplying branch perfusion may be in systole. In general, a branch that originates exclusively from the aortic false lumen is rarely affected by an ischemic complication.
Consistently, the aortic septum prolapses with a convex contour
an obliterated aortic true lumen that supplies the compromised branches is most expeditiously and effectively approached by an endovascular aortic procedure rather than a strategy directed at the individual branches.
More than one mechanism of branch involvement can coexist in any given patient. The clinical manifestations and the analysis of imaging for any patient requires an individualized approach that must synthesize information and aortic and branch vessel involve­ment to customize an optimal treatment strategy that will safely, successfully, and durably address the most compelling effects of the dissection.
toward a compromised crescent-shaped true lumen. Consequently, all branches originating from the true lumen are at risk of obstruc­tion. In this regard, the aortic septum in a dynamic obstructive process often assumes a coronal position, oriented across the aorta from left to right, in the distal descending thoracic proximal abdominal aortic segments. Consequently, the anteriorly oriented mesenteric vessels are in peril of ischemia because they frequently originate exclusively from a miniscule aortic true lumen. The like­lihood of developing clinically relevant dynamic branch vessel compromise appears related in part to the area of the proximal entry tear. Although the process of dynamic involvement is depen­dent on multiple factors, as a general rule, the more severe the true lumen collapse, the larger or more circumferential the size of the proximal primary entry tear. Management of more than one ischemic vascular bed related to dynamic branch involvement and
Aortic Interventions
Endovascular aortic stent grafting is a less invasive alternative to open surgery for selected patients with both thoracic and abdomi­nal aneurysms. Recently, the application of similar technology for management of acute aortic syndromes, including aortic dissec­tion, has emerged as a focus of interest and study. any new procedure, the key question is the determination of spe­cific patient populations who may benefit from the new technique. In this regard, the use of traditional classification parameters for risk stratification of aortic dissection patients has advanced evalu­ation of the possible benefits and risks of endograft management.
Nearly all experience in endograft management of aortic dissection has been with type B disease when there is exclusive
7,10–13,20,21
As with
involvement of the descending thoracic aorta. Experience with
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endograft applications in type A dissection is limited to isolated case reports. In the United States, type B aortic dissections consti­tute approximately 30% to 35% of all dissections. The initial risk stratification of the type B dissection is made with the determina­tion of the presence or absence of complications.
Medical management is the traditional treatment strategy for uncomplicated acute aortic dissection. Current reports cite a 30-day mortality rate of approximately 10%.
22,23
Use of stent grafting for stable uncomplicated patients with type B aortic dissection has yet to realize any improvement in survival compared to traditional medical therapy. Indeed, current conservative noninterventional management of uncomplicated cases is associated with 1-year sur­vival rates of around 80%. Such results may be hard to improve upon with endograft therapy.
23,33
Stent Grafts for Uncomplicated Type B Dissection
The Investigation of Stent Grafts in Patients with Type B Aortic Dissection (INSTEAD) trial observed that elective stent graft place­ment in survivors of uncomplicated chronic type B dissection does not improve 1-year survival and adverse event rates com­pared with medical therapy. Among the 140 patients randomized in this prospective trial, 1-year survival was 91% compared with 97% in patients randomized to medical therapy. related mortality was not different, and the risk for the combined endpoint of aorta-related death (rupture) and progression (includ­ing conversion or additional endovascular or open surgical inter­vention) was similar.
In the setting of complicated aortic dissection, medical manage­ment is associated with a high mortality rate, such that most patients will undergo surgery to address life-threatening complications. Depending on the patient's underlying medical conditions and the nature of the complication(s), surgical mortality rates range from between 30% and 60% or higher.
24,25
It is in these high-risk scenar­ios that an opportunity exists to establish a role for interventional management. Thus the question becomes, What constitutes compli- cated type B aortic dissection? There is no strict definition for this category of disease, but traditionally it is relegated to two unam­biguous disease manifestations: aortic rupture ( tomatic branch vessel involvement. These conditions are clear and their diagnosis unequivocal. Other adverse effects of the dissection process, such as uncontrollable hypertension, unrelenting pain,
34,35
Moreover, aorta-
Fig. 36-7) and symp-
2,4
and increasing pleural fluid, defy easy classification and do not have uniform criteria for comparative assessment. These so-called softer indications for intervention are commonly included as a surgical indication in most published series of acute complicated dissection.
8,26
Endograft Treatment of Complicated Type B Dissection
The procedural goal for endovascular stent grafting in patients with complicated acute type B aortic dissection is endograft elimi­nation of blood flow entry into the proximal entry tear. Obliterating the primary communication between the true lumen and the false redirects pulsatile flow into the true lumen, promotes false lumen thrombosis, and ultimately improves remodeling of the aorta by increasing the dimensions of the true lumen while shrinking the false lumen (
Fig. 36-8).
Specific procedural techniques vary depending on the precise complication. Faced with dynamic branch vessel involvement and clinically relevant obstruction compromising flow to one or multiple branches, the procedural strategy focuses on unload­ing the aortic false lumen by increasing resistance to false lumen inflow or decreasing resistance to its outflow. The former is attempted by deploying an endograft over the proximal pri­mary entry tear and rechanneling all flow into the true lumen. Logistically, this typically involves placement of a 15-cm-long (range 12-20 cm) stent graft from the nondissected segment of aorta proximal to the primary intimal tear, commonly between the origins of the left carotid and left subclavian arteries. This may require intentional partial or complete coverage of the left subcla­vian origin. The distal extent of the device usually remains above the diaphragm. The diameter of the implant selected is based on the transaortic dimension of the nondissected aorta just proximal to the dissection, rather than the size of the true lumen or trans­aortic diameter of the dissected segment.
Endovascular Treatment of Branch Vessel Involvement
The outcomes of stent graft therapy for reversal of dynamic branch vessel involvement are excellent, with procedural success in up to 95% of cases and complete false lumen thrombosis in 85% of patients. freedom from aortic rupture and open repair.
7–9
These procedures are associated with 67.7% 5-year
9
Additionally, static
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A B C
FIGURE 367 Acute type B aortic dissection with rupture in a 68-year-old woman. A, Frontal chest radiograph upon presentation to emergency room with severe back pain and hypertension that occurred while gardening. B, Axial computed tomography (CT) scan after contrast media administration shows typical appearance of aortic dissection in mid-descending aorta. C, Repeat chest radiograph performed after transfer to referral facility 4 hours after initial study, with marked interval change including opacification of left hemithorax from leaking blood.
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FIGURE 368 Treatment and follow-up imaging of type B aortic dissection with rupture. A, Aortograms pre- and post placement of a thoracic endograft across mid-descending aorta entry tear of a type B dissection in the 68-year-old woman described in Figure 36-7. B, Series of axial computed tomography (CT ) images obtained 1 week postendograft management of a type B dissection with rupture. Stent graft is in good position, and false lumen is thrombosed. Residual extravascular blood and hematoma are evident.
branch involvement remote from the covered proximal aortic entry tear may require separate targeted intervention to manage residual ischemic compromise. This is especially important in cases with no-reentry anatomy complicating static branch involve­ment. In these situations, endovascular branch intervention should be provided emergently.
An alternative to endograft placement in dynamic branch
compromise is distal flap fenestration.
9,27
Percutaneous bal­loon fenestration of the aortic septum has replaced the opera­tive procedure. Balloon fenestration of the septum is designed to unload the aortic false lumen by decreasing the resistance to outflow. Technically, initial transgression of the aortic flap with a small cardiac transseptal TIPS needle and cannula usually is
performed from the small true lumen into the larger target of the false channel. The site of the needle puncture commonly lies within the infrarenal aorta at the level of the aortic bifurcation. Once successful transgression of the septum is confirmed, a wire is advanced across the flap and well into the targeted lumen. Sequentially larger balloon dilation of the flap is performed until a final size of between 20 and 25 mm is obtained.
Balloon fenestration causes a linear transverse tear in the flap that allows greater mixture of blood between the two aortic chan­nels and decompresses the true lumen. These effects must be confirmed by aortography or intravascular ultrasound (IVUS) to ensure relief of the dynamic pattern of branch obstruction. After these two endovascular (endograft or fenestration) procedures,
imaging comparisons of the anatomical effects (with computed
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tomography [CT], magnetic resonance imaging [MRI] or IVUS), including changes in the size of the aortic lumens, typically dem­onstrate a more dramatic result following endograft management. Specifically, the magnitude of true lumen expansion with stent grafting is greater than that observed after distal flap fenestration. Because false lumen fenestration promotes flow in the false lumen, whereas endograft placement promotes false lumen thrombosis, the latter is thought to be a superior method to minimize late aneu­rysm formation. Consequently, the opportunities for percutaneous balloon fenestration are decreasing now that thoracic endograft availability has improved. Fenestration is typically limited to situa­tions when stent grafts are unavailable or when the specific aortic anatomy is unsuitable for endograft placement.
Aortic Rupture
Rupture that complicates aortic dissection is an interventional imperative. focus on preventing exsanguination. Both open surgical and endo­vascular therapies are associated with high mortality and morbi­dity rates in the presence of aortic rupture. Recent reports suggest
28,29
The procedural considerations for aortic rupture
that endovascular approaches permit treatment of more patients, including older and less fit individuals whose operative risk in this setting is prohibitive.
21,28,29
Localizing the precise site of rupture noninvasively is not always possible. The point of rupture through the false lumen wall may be evident by the presence of contrast enhancement beyond the anticipated aortic border, though this occurs typically in the set­ting of severe hemodynamic instability or shock (
Fig. 36-9). More
commonly, a periaortic, mediastinal, and/or pleural collection is evident on CT imaging, which has an appearance and attenua­tion value consistent with hematoma or complex fluid. This abnor­mality may be most prominent around a focal aortic segment or extend diffusely over a wider zone.
The goal of endograft management for aortic rupture is cover­age of the proximal entry tear, with isolation of the false lumen, to ensure false lumen obliteration and expeditious thrombosis. It is thrombosis of the false lumen that prevents aortic leakage of blood. To facilitate rapid false lumen thrombosis, the overall endograft coverage of the aorta is often longer than that used for other thoracic pathologies. By extending the length of coverage (20-30 cm) to at least the level of the diaphragm or celiac trunk, the aortic septum is braced by the stent in the true lumen, and the
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B
FIGURE 369 Endograft management of aortic dissection with rupture. A, Axial and sagittal computed tomography (CT ) images of 59-year-old man with acute type B dissection with primary tear distal to left subclavian artery and retrograde extension into the proximal arch (DeBakey class IIID) complicated by rupture. Axial projection shows a large quantity of extravascular fluid, and sagittal image shows a faint wisp of contrast extravasation above aorta, just distal to subclavian artery. B, Three views from the stent graft procedure, with the left and middle panels before device placement, and the right panel after deployment. A good result is evident, with contrast opacification of the true lumen only.
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