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Chapter Physiopathology of Ischemic Complications of Aortic Dissections 23 David M. Williams, Bora Peynircioglu Contents 23.1 Introduction . . . . . . . . . . . . . . . . . . . . . . . 239 l Classification of branch artery obstruction l Clinical diagnosis of malperfusion l Setting priorities and avoiding pitfalls. 23.2 Identification of the True and False Lumens . . . . . 239 23.3 Importance of Abdominal Aortic Dissection . . . . . 240 23.4 Classification of Branch Artery Obstruction . . . . . 241 23.5 Diagnosis of Branch Artery Obstruction . . . . . . . 242 23.6 Setting Priorities and Avoiding Pitfalls . . . . . . . . 243 23.7 Conclusion . . . . . . . . . . . . . . . . . . . . . . . . . 243 23.1 Introduction Acute aortic dissection typically kills by tamponade or exsanguination owing to false-lumen rupture or by organ ischemia owing to the malperfusion syndromes [4, 8, 9, 12, 13]. Until recently, the purview of angiography was treating the malperfusion syndromes, with the goal of restoring flow to obstructed arteries and treating medically the ensuing reperfusion injury as best we could. This treatment consisted of fenestration and deployment of uncovered stents on the basis of complete evaluation of the aorta and critical branch arteries, as directed by the clinical examination of the patient, intravascular ultrasound survey of the aorta, and branch arteriography and manometry. The availability of endografts initiated the opportunity of treating the malperfusion syndromes more expeditiously and, in addition, preventing rupture by inducing thrombosis of the false lumen [3, 5, 10, 11]. As in any medical endeavor, errors in diagnosis lead to errors in treatment. The goals of this chapter are to survey the mechanisms by which aortic dissection leads to organ or limb malperfusion and to consider a few of the pitfalls in establishing the diagnosis. In particular, the discussion of malperfusion in the setting of aortic dissection will be divided into these topics: l Identification of the true and false lumens l Importance of abdominal aortic dissection 23.2 Identification of the True and False Lumens Identification of the true and false lumens is crucial in the endovascular treatment of aortic dissection. The true and false lumens behave differently. In most acute aortic dissection, the false lumen is prone to ectasia and is at risk of rupture, and the true lumen is prone to collapse and is at risk of compromise of its branch arteries. Numerous steps in the endovascular treatment of dissection require real-time knowledge of which lumen the guidewire, the diagnostic catheter, and treatment devices lie within. These steps include: l Deploying an endograft across the entry tear within the true lumen l Stenting a branch artery to the aortic true lumen l Stenting the aortic true lumen after fenestration, to reduce a prolapsing flap l Aligning both iliac arteries with the aortic true lumen during aortoiliac stenting l Avoiding complicating future transfemoral catheter procedures, retrograde aortic perfusion, or endograft treatment because of injudicious placement of aortic or branch artery stents. In chronic dissections, the distinction between the true and false lumens is usually straightforward. For most of these patients, the interventionalist will have the benefit of a chest, abdomen, and pelvis computed tomography (CT) scan. In acute dissections, a complete CT examination may not be available. Features identifying the false lumen include aortic cobwebs and the ªbeakº sign [6, 7, 14]. Aortic cobwebs are remnants of media stretching (like cobwebs) between the dissection flap and the outer wall of the false lumen (Fig. 23.1). The beak sign is the acute angle by which the dissection flap meets the outer wall of the aorta (Fig. 23.1). As 240 IV. Dissection b Fig. 23.1. Cordlike remnants of media, ªaortic cobwebs,º are a reliable marker of the false lumen (a, arrows). Characteristically, they stretch from the dissection flap covering the true lumen (a, arrowheads) to the outer wall of the false lumen). On the computed tomography examination of this patient, a cobweb is visible in the distal thoracic aorta (b, arrow). The acute angle or ªbeakº (b, arrowhead) marks the junction of the dissection flap with the aortic wall and lies within the false lumen a a b c Fig. 23.2. Two distinct lumens are present in the thoracic aorta (a) and in the common iliac arteries (b). In the intervening abdominal aorta, the second lumen has nearly disappeared (c). Here, the true lumen has collapsed completely and is visible as a curvilinear filling defect along the anterior margin on the aorta (c, arrow), where it lies across the origin of the superior mesenteric artery (asterisk) such, this angle (or beak) is the imaging correlate of the cleaving wedge of hematoma which splits the medial layers to form the false lumen. These signs are highly reliable identifiers of the false lumen. Generally reliable characteristics of the true lumen are continuity with the aortic root, which remains the source of the majority of the large-diameter aortic branches, and continuity with the femoral arteries. Once the lumens have been identified, they should be traced from root to groin. A reliable anatomical rule to use while drawing a mental path within the aorta from slice to slice on a CT examination is that every time the path crosses the flap it changes the lumen. A second reliable anatomical rule is that, in acute dissections, the lumens are continuous. If two lumens are observed in the chest and two are observed in the pelvis, then two are present in the abdomen, although one of them may be difficult to identify (Fig. 23.2). Sources of branch artery perfusion are identified as exclusively true lumen, exclusively false lumen, or shared true and false lumens. Branches with shared perfusion are further characterized as with or without reentry tears. 23.3 Importance of Abdominal Aortic Dissection Renal, mesenteric, or spinal cord malperfusion approximately doubles the mortality of patients with acute aortic dissection [2]. Most of these malperfusion syndromes arise as complications of the dissection path through D. M. Williams, B. Peynircioglu Fig. 23.3. A single lumen is prominent at the level of the aortic crura near the diaphragm in the same patient as in Fig. 23.2. Careful tracing of this lumen back to the heart shows that it is the false lumen, and that the true lumen is completely collapsed and nearly invisible. Until proven otherwise, the bowel must be considered at risk. The true lumen has collapsed against the anterior wall of the aorta, scalloping the anterior margin of the false lumen the abdominal aorta, the source of the critical branch arteries. Because of its crucial prognostic role, separate discussion of the abdominal aorta is worthwhile. The false lumen which tapers and disappears at the diaphragm may be of little consequence; however, the true lumen which tapers and disappears at this location represents a lethal, if not mortal, injury (Fig. 23.3), because every true lumen branch distal to the disappearing flap is at risk of obstruction and end-organ infarction. In some cases, the true lumen is so completely collapsed that it is visible only as a scalloping of the anterior aortic lumen (Fig. 23.3). If a lumen ªendsº at the diaphragm, make sure it is the false lumen, not the true lumen. 23.4 Classification of Branch Artery Obstruction The Michigan classification of branch artery obstruction [15] is based on the anatomical relationship of the dissection flap to the branch artery in question (Fig. 23.4). It is an intuitively appealing classification because this anatomic distinction forms the basis of distinct treatment strategies. The causes of obstruction may be distinguished as follows: l Static obstruction l Dynamic obstruction l Mixed static and dynamic obstruction l Miscellaneous ± Related to dissection: thrombosis, embolism ± Unrelated to dissection: atherosclerosis, fibromuscular dysplasia. Chapter 23 Physiopathology of Ischemic Complications of Aortic Dissections Fig. 23.4. Anatomical drawing, static vs dynamic obstruction. Reprinted with permission [19] In static obstruction, the dissection flap intersects the origin of a branch and potentially encroaches on the lumen. If the dissection enters the vessel origin but does not reenter, the true lumen of the vessel is narrowed, and a pressure gradient may be measured across the stenosis between the aorta and the arterial trunk. If the false lumen reenters through a large enough tear, it can completely compensate for a narrowed true lumen, and no pressure gradient may be present. Treatment is aimed at relieving the branch artery stenosis. In dynamic obstruction, the dissection flap spares the vessel origin, but prolapses across it like a curtain. This obstruction is dynamic in two senses. It is observed only during cross-sectional imaging with the aorta pressurized and conducting flow; it disappears when the aorta is observed at aortotomy or at necropsy (Fig. 23.5). Furthermore, it may disappear during medical treatment with antihypertensives and beta-blockers, and recur when medications are discontinued (Fig. 23.6). Treatment must be directed at the dissection flap in the aorta. Static and dynamic obstruction can simultaneously contribute to branch artery obstruction. In addition, complete occlusion of a vessel by either mechanism can lead to thrombosis of the true lumen distally. In the kidney, which has no effective collateral supply, this can lead to diffuse renal branch artery thrombosis, an unsalvageable condition. In the pelvis, iliac artery thrombosis is often arrested at the iliac bifurcation, where collateral supply from lumbar arteries or the contralateral internal iliac artery reconstitutes the obstructed internal and external iliac arteries. A false lumen which thromboses without a reentry tear can completely fill an artery (or even the aorta), effectively obliterating the true lumen. Furthermore, retrograde thrombosis beginning distally in the vessel can proceed to complete occlusion of that vessel. We have observed this in the iliac, renal, and superior mesenter- 241 242 IV. Dissection a b c Fig. 23.5. a Computed tomography shows collapse of the true lumen against the anterior wall of the abdominal aorta, occluding the superior mesenteric artery (SMA). Small rulers were inserted medially into the false lumen on the autopsy specimen (b) up to the anterior margins of the dissection. These confirm that the dissection flap spared the SMA origin, despite diffuse bowel infarction (c) Fig. 23.6. A patient with acute type B dissection was being evaluated for renal artery involvement. Intravascular ultrasound when the patient was at her well-treated normotensive state (a) of 90/50 showed a capacious true lumen with unimpeded SMA perfusion. During treatment for impending sedation-induced respiratory arrest, her pressure was driven up to 159/83, resulting in collapse of the true lumen and obstruction of the SMA (b). When her pressure returned to the baseline, the true lumen also returned to its baseline state, reopening the SMA (c). The dissection flap is marked by arrowheads ic arteries. When it occurs in the aorta, the patient may present with symptoms of spinal cord ischemia. A true lumen may thrombose distal to a dissection flap which covers yet does not enter the vessel origin. This occurs most often in the common iliac artery, when the dissection spares one common iliac origin but enters the other. Complete stasis is present on the nondissected side, and thrombosis ensues. Cross-pelvic collaterals from the contralateral dissected side generally arrest this thrombosis at the iliac artery bifurcation. When the iliac artery is completely thrombosed, it may be difficult to tell whether the thrombosis is within the true or the false lumen, but the distinction is crucial. When thrombosis is present in the false lumen, the obstruction may be treated by means of a stent in the true lumen. When the thrombosis is in the true lumen, the thrombosis must be cleared by mechanical or other thrombolysis before flow in the true lumen is restored by endograft or fenestration. Embolic occlusion of false and true lumen branches is unusual. Embolism to false lumen branches usually originates from thrombus poorly adhering to the dissection flap. Embolism to true lumen branches usually originates from thrombus forming in regions of stasis, as outlined in the previous paragraph. Other sources include thrombus on the true lumen side of the dissection flap forming at sites of spontaneous reentry tears, or from thrombus within a false lumen extruded into the true lumen through an iatrogenic reentry tear during an angioplasty or stent delivery. Special situations are beyond the scope of this chapter. These include presentation of dissection and malperfusion in patients with a prior aortic endograft or interposition graft, causes of malperfusion in patients with aortic dissection unrelated to the dissection flap, and causes of malperfusion in patients with previous negative angiographic workup. 23.5 Diagnosis of Branch Artery Obstruction Cross-sectional imaging is useful to ruling out ªischemic anatomy.º If the true lumen is of reasonable caliber from entry tear to termination, and if the dissection flap spares every major branch artery, branch artery obstruction is unlikely. However, if the flap crosses a vessel origin, or the true lumen is collapsed, malperfusion may be present, and should be evaluated by angiography. Evaluation begins with inspection of the flap in relation to branch artery origins. This can be done most expeditiously using intravascular ultrasound. Pressure measurements are made simultaneously in the aor- D. M. Williams, B. Peynircioglu a Fig. 23.7. Pressure tracings at the level of the SMA from the patient in Fig. 23.3. True and false lumen pressures are nearly equal (a), despite nearly total collapse of the true lumen. In Chapter 23 Physiopathology of Ischemic Complications of Aortic Dissections b contrast, a profound pressure deficit is present in the SMA, which arises exclusively from the true lumen (b). TL true lumen, FL false lumen a b c d Fig. 23.8. Pressures. No aortorenal gradient is present in the proximal renal artery (a). However, the renal artery injection shows that the dissection flap (arrow) extends to the renal hilum (b), and so the proximal renal artery pressure may not re- flect renal perfusion pressure. A catheter in the true lumen distal to the dissection (c) documents a small aortorenal pressure gradient (d). Other renal branches may be subject to different deficits in perfusion pressure tic root and abdominal aortic true and false lumens. If these are equal, subsequent pressure measurements can be made using the abdominal aortic pressure as a surrogate for root pressure. If they are unequal, then a search for a pressure drop across a coarctation-like obstruction within the aorta should be made. Aortic pressures should be compared with arterial trunk pressures in the organ of clinical concern as well as in those branches suspected of being compromised on the basis of imaging. Equal pressures in a false lumen and a collapsed true lumen do not mean that the branch artery pressures are also equal (Fig. 23.7). Pressure measurements should be made within the branch artery of interest. Furthermore, branch artery manometry should be followed by selective arteriography, to make sure that measurements are representative of per- 243 244 IV. Dissection fusion pressure at the organ level. This precaution is necessary in instances of static obstruction, wherein the reentry tear may be several centimeters deep in the trunk; unless the measurement is distal to the reentry tear, it may underestimate the branch artery deficit in perfusion pressure (Fig. 23.8). As already noted, dynamic obstruction may be demonstrably pressure-dependent (Fig. 23.6). An occasional scenario is the patient who arrives in the emergency department with tearing chest pain, loss of leg pulses, and refractory hypertension, is aggressively treated with antihypertensives and beta-blockers, and finally arrives, chatty and serene, in the angiography suite to rule out malperfusion. In cases such as this, especially when the clinical history suggests the patient is noncompliant with medications or clinical follow-up, a negative workup for malperfusion is followed by reassessment after tapering down the dose of the beta-blocker. For this reason, we request patients with subacute dissection and a history suggesting sporadic episodes of malperfusion be converted to short-acting beta-blockers, antihypertensives, and sedation. Patients with acute dissection are, ordinarily, already being treated with short-acting drugs. whom aortic root reconstruction may be delayed. For example, deploying a Wallstent through a fenestration tear, from the false lumen above to the true lumen below, may effectively treat the malperfusion. However, by compressing the true lumen adjacent to the false lumen component of the Wallstent, this procedure greatly complicates future transfemoral access to the brachiocephalic vessels and may preclude future cardiac bypass using retrograde transfemoral perfusion. Instead, the stent should be deployed entirely within the aortic true lumen. A similar consideration in patients with acute type A dissection complicated by malperfusion is pertinent to creation of the circumferential tear in the flap during the so-called scissor technique [1]. 23.7 Conclusion The malperfusion syndromes greatly increase the mortality of acute aortic dissection. Endovascular techniques, if timely and if carried out with clear and complete understanding of the vascular pathoanatomy of the individual patients, are highly successful in correcting malperfusion. 23.6 Setting Priorities and Avoiding Pitfalls The leaking false lumen (which heralds impending rupture or tamponade) and florid aortic insufficiency take precedence over malperfusion, and are indications for immediate open repair in patients with reasonable operative risk. The De Bakey and Stanford classifications provide straightforward anatomical criteria for stratifying patients into immediate surgical or medical management. Patients with prolonged malperfusion of gut or lower extremity may be unsuitable for immediate repair even with type A dissection, and in such cases immediate therapy is directed at restoring flow to critical vessels. The mechanism of arterial obstruction determines the appropriate treatment in a given case, and so the first principle of treatment is to define arterial anatomy and assess visceral perfusion. In particular, assuring the integrity of the superior mesenteric artery, or restoring perfusion to the compromised superior mesenteric artery, has the highest priority of any endovascular goal in this group of patients. Even when resection of dead bowel is necessary, preoperative endovascular restoration of superior mesenteric artery perfusion will give the general surgeon reliable margins between uncompromised and unsalvageable bowel. 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