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Green GR, Kron IL. Aortic Dissection.
In: Cohn LH, Edmunds LH Jr, eds. Cardiac Surgery in the Adult. New York: McGraw-Hill, 2003:10951122.

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Chapter 45

Aortic Dissection

G. Randall Green/ Irving L. Kron

HISTORY
CLASSIFICATION
INCIDENCE
ETIOLOGY AND PATHOGENESIS
ACUTE AORTIC DISSECTION
????Clinical Presentation
????????SIGNS AND SYMPTOMS
????????DIAGNOSTIC STUDIES
????????DIAGNOSTIC IMAGING
????????DIAGNOSTIC STRATEGY
????Natural History
????Initial Medical Management
????Operative Indications
????Operative Technique
????????ANESTHESIA AND MONITORING
????????HEMOSTASIS
????????CARDIOPULMONARY BYPASS
????????CEREBRAL PROTECTION
????????TECHNIQUES FOR TYPE A DISSECTION
????????TECHNIQUES FOR TYPE B DISSECTION
????????MALPERFUSION SYNDROME
????Postoperative Management
????Long-term Management
????Results
CHRONIC AORTIC DISSECTION
????Clinical Presentation
????????SIGNS AND SYMPTOMS
????????DIAGNOSTIC IMAGING
????Natural History
????Operative Indications
????Operative Technique
????????GENERAL CONSIDERATIONS
????????CEREBRAL AND SPINAL CORD PROTECTION
????????TECHNIQUES FOR TYPE A DISSECTION
????????TECHNIQUES FOR TYPE B DISSECTION
????Results
CONCLUSION
REFERENCES

?? INTRODUCTION
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Thoracic aorta dissection occurs as blood flow is redirected from the aorta (true lumen) through an intimal tear into the media of the aortic wall (false lumen). A dissection plane that separates the intima from the overlying adventitia along a variable length of the aorta is created within the media. The acute form of aortic dissection is often rapidly lethal, while those surviving the initial event go on to develop a chronic dissection with more protean manifestations. The purpose of this chapter is to review the etiology and pathogenesis of aortic dissection, examine current diagnostic algorithms, and provide detailed descriptions of contemporary surgical techniques for treatment. Additional information regarding follow-up and the subsequent management of these patients is presented to provide a comprehensive understanding of a clinical entity that has challenged physicians and surgeons for centuries.


?? HISTORY
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Sennertus is credited with the first description of the dissection process, but the earliest detailed descriptions of the clinical entity appeared in the 17th and 18th centuries, during which time Maunoir named the process aortic "dissection."1,2 Laennec defined the propensity of the chronically dissected aorta to become aneurysmal.3 Aortic dissection was exclusively a postmortem diagnosis until the first part of the 20th century, but in 1935 Gurin attempted surgical intervention with the first aortic fenestration procedure to treat malperfusion syndrome.4 In 1949 Abbott and Paulin advanced surgical treatment by theoretically preventing aortic rupture by wrapping the aorta with cellophane.5 Other attempts at surgical treatment over the years met with limited clinical success while certain concepts regarding surgical management are still in use today. With the advent of cardiopulmonary bypass, DeBakey and Cooley forever altered the natural history of aortic dissection by successfully performing primary surgical repair using techniques not remarkably different from contemporary procedures.6,7 Investigators such as Wheat made substantial contributions by defining physiologically based medical management algorithms to complement surgical correction.8 There is still considerable controversy regarding surgical versus medical treatment of certain forms of acute thoracic aortic dissection.


?? CLASSIFICATION
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The classification systems used for aortic dissection are based on the location and extent of dissection. The particular type is then subclassified based on the timing of dissection. Acute dissection has traditionally been used to describe presentation within the first 2 weeks, while the term chronic is reserved for those patients presenting at greater than 2 months following the initial event. The more recently added subacute designation is sometimes used to describe the period between 2 weeks and 2 months.

Two classification systems are most frequently used in clinical practice: the DeBakey and the Stanford systems (Fig. 45-1). The DeBakey system differentiates patients based upon the location and extent of aortic dissection.9 The advantage of this system is that four different groups of patients with different forms of aortic dissection emerge and provide the greatest opportunity for subsequent comparative research. In contrast, the Stanford system proposed by Daily et al is a functional classification system.10 All dissections that involve the ascending aorta are grouped together as type A, regardless of where the primary tear occurs. Proponents of the simpler Stanford system contend that the clinical behavior of patients with aortic dissection is essentially determined by involvement of the ascending aorta. Critics, however, suggest that individual patients in the type A classification may be quite different from one another depending upon the distal extent of dissection. Drawing clinical conclusions from such a potentially heterogeneous patient population has inherent limitations. The Stanford system will be used throughout this chapter.



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FIGURE 45-1 Classification of aortic dissection. DeBakey type I and Stanford type A include dissections that involve the proximal aorta, arch, and descending thoracic aorta. DeBakey type II only involves the ascending aorta; this dissection is included in Stanford type A. DeBakey type III and Stanford type B include dissections that originate in the descending thoracic and thoracoabdominal aorta regardless of any retrograde involvement of the arch. These are subdivided into a and b depending on abdominal aortic involvement. (Reproduced with permission from Stone C, Borst H: Dissecting aortic aneurysm, in Edmunds LJ Jr (ed): Cardiac Surgery in the Adult. New York, McGraw-Hill, 1997; p 1125.)

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?? INCIDENCE
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Aortic dissection is the most frequently diagnosed lethal condition of the aorta and occurs nearly three times as frequently as does rupture of abdominal aortic aneurysm in the United States.11 There is an estimated worldwide prevalence of 0.5 to 2.95 per 100,000 per year; the prevalence ranges from 0.2 to 0.8 per 100,000 per year in the United States, resulting in roughly 2000 new cases per year. These figures are, however, only an estimate. In one autopsy series, the antemortem diagnosis was made in only 15% of patients, revealing that many immediately fatal events go undiagnosed.12 Clinically, type A dissections occur with an overall greater frequency (Table 45-1).


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TABLE 45-1 Clinical characteristics of patients presenting with acute type A and B thoracic aortic dissections

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?? ETIOLOGY AND PATHOGENESIS
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There are several hypotheses regarding the etiology of the intimal disruption (primary tear) that permits aortic blood flow to create a cleavage plane within the media of the aortic wall. This was originally viewed as a consequence of a biochemical abnormality within the media upon which normal mechanical forces in the aorta acted to create an intimal tear. The link between the abnormal media, termed cystic medial necrosis or degeneration, and the primary tear has not been scientifically established. In fact, medial degeneration is found in only a minority of patients with acute aortic dissection and most are children.13 This theory has lost support over the years.

Alternatively, there are data supporting a relationship between aortic dissections and intramural hematoma. Advocates of this theory suggest that bleeding from vasa vasorum into the media creates a mass, which results in localized areas of increased stress in the intima during diastole. These areas then permit intimal disruption. In fact, between 10% and 20% of patients thought to have acute aortic dissection are found to have intramural hematoma suggesting that it may be a precursor to dissection.14 Penetrating atherosclerotic ulcers have been implicated as the source of intimal disruption in certain cases, yet support for the concept has waned over the years. The pattern of atherosclerotic involvement of the thoracic aorta resulting in penetrating ulcer and the frequency of dissection throughout the aorta do not support this theory.

While no single disorder is responsible for aortic dissection, several risk factors have been identified that can damage the aortic wall and lead to dissection (Table 45-2). These include direct mechanical forces on the aortic wall (i.e., hypertension, hypervolemia, derangements of aortic flow) and forces that affect the composition of the aortic wall (i.e., connective tissue disorders or direct chemical destruction). Hypertension is the mechanical force most often associated with dissection and is found in greater than 75% of cases. Although the role of increased strain on the aortic wall is intuitive, the mechanism by which hypertension actually leads to dissection is unclear. Similarly, hypervolemia, high cardiac output, and an abnormal hormonal milieu certainly contribute to the increased incidence of dissection in pregnancy, but the mechanism is unclear. Atherosclerosis is not a risk factor for aortic dissection except in preexisting aneurysms or in the case of atherosclerotic ulceration, which may lead to dissection in the descending thoracic aorta. Iatrogenic trauma to the aortic intima may result in dissection. Catheterization procedures, aortic root and femoral artery cannulation for cardiopulmonary bypass, aortic cross-clamping, surgical procedures performed on the aorta (aortic valve replacement and aorto-coronary bypass grafting), and placement of intra-aortic balloon pumps have all been reported to result in dissection. Aortic transection as a result of trauma rarely results in excessive dissection and deserves differentiation from the process of aortic dissection. This process is usually limited to the aortic isthmus and in addition to the risk of rupture may present as a circular prolapse of the intima and media producing aortic obstruction referred to as "pseudo-coarctation" (Fig. 45-2).


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TABLE 45-2 Risk factors for type A and B thoracic aortic dissection

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FIGURE 45-2 Axial image of CT arteriogram showing a nearly circumferential dissection flap (arrowhead) as a result of acute traumatic aortic transection. (Reproduced with permission from Stone C, Borst H: Dissecting aortic aneurysm, in Edmunds LJ Jr (ed): Cardiac Surgery in the Adult. New York, McGraw-Hill, 1997; p 1125.)

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Once a cleavage plane exists in the media, the aortic wall floating within the lumen is termed the dissection flap and is composed of the aortic intima and partial thickness media. The primary tear is usually greater than 50% of the circumference of the aorta, but the full circumference is rarely involved. The primary tear in type A dissection is usually located on the right anterior aspect of the ascending aorta and follows a somewhat predictable course, spiraling around the arch and into the descending thoracic and abdominal aorta on the left and posteriorly. The dissection may propagate in a retrograde fashion for a variable distance as well to involve the coronary ostia; this occurs in roughly 11% of all dissections.15 Myocardial ischemia and rupture into the pericardium are the cause of death in as many as 80% of deaths from acute dissection. Often the distal false lumen communicates with the true lumen through one or more fenestrations within the dissection flap. The false lumen may also end blindly in as many as 4% to 12% of patients, in which case blood in the false lumen frequently becomes thrombotic. The false lumen may also penetrate the adventitia causing rupture and death. Regardless of whether the true and false lumen communicate, perfusion of aortic side branches may be compromised by the dissection causing end-organ ischemia (Fig. 45-3). If these acute complications are avoided, the weakened outer aortic wall, composed of partial media and the adventitia, may dilate over time resulting in aneurysm formation. This long-term complication is the reason for operation in the majority of chronic dissections regardless of type.



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FIGURE 45-3 Diagram of aortic dissection. (A) An intact dissection membrane compresses the true lumen and causes malperfusion of a branch artery. (B) Rupture of the dissection membrane that may or may not restore blood flow to the branch.

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The adventitia provides most of the tensile strength of the aortic wall with little contribution from the media. The media is composed of concentrically arranged smooth muscle interposed with connective tissue proteins such as collagen, elastin, and fibrillin within the ground substance. Abnormal constituents of the media, as in certain connective tissue disorders such as Marfan disease and Ehlers-Danlos syndrome, are associated with aortic dissection. Marfan syndrome is an autosomal dominant inherited disorder in which a point mutation in the fibrillin-1 gene (FBN1) located on the long arm of chromosome 15 results in an abnormal media. The incidence of Marfan syndrome is approximately 1 per 5000 live births. There are, however, many incomplete forms of the disease and as many as 25% may be sporadic in which no known fibrillin abnormalities are observed. Type IV Ehlers-Danlos syndrome is a connective tissue disorder of the pro{alpha}1(III) chain of Type III collagen with an incidence of 1 in 5000. The structurally abnormal media is susceptible to dissection. There are also familial aggregations of dissection without discernable biochemical or genetic abnormalities.


?? ACUTE AORTIC DISSECTION
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Clinical Presentation

SIGNS AND SYMPTOMS

As many as 40% of patients suffering acute aortic dissection die immediately. Those surviving the initial event may be stabilized with medical management, and it is these patients in whom subsequent therapeutic intervention of aortic dissection has altered the natural history of the disease. The clinical outcome is eventually determined by dissection type and timing of presentation, patient-related factors, and the quality and experience of the individuals and institution providing care.

The initial evaluation of a stable patient suspected of having aortic dissection includes a detailed history and physical examination focusing on those elements likely to rule in the diagnosis. The diagnosis of aortic dissection requires a high level of suspicion. As many as 30% of patients ultimately diagnosed with acute dissection are first thought to have another diagnosis. Aortic dissection should always be considered in the setting of severe, unrelenting chest pain, which is present in most patients. Patients usually have no previous episodes of similar pain and are often quite anxious. Pain is generally located in the mid-sternum for ascending aortic dissection and in the interscapular region for descending thoracic aortic dissection (see Table 45-1). It is not unusual for the location of maximum pain to change as the dissection extends in an antegrade or retrograde direction and such "migratory pain" should arouse clinical suspicion. The character of the pain is often described as "ripping" or "tearing" and is constant with greatest intensity at the onset. Painless dissection has been described and usually occurs in the setting of an existing aneurysm where the pain of a new dissection may not be differentiated from chronic aneurysm pain. Patients may also have signs or symptoms related to malperfusion of the brain, limbs, or visceral organs. These findings may dominate the presentation following an initial episode of pain.

Elements of the past medical history such as primary hypertension, presence of aneurysmal disease of the aorta, or familial connective tissue disorders are useful as risk factors to help establish the diagnosis. Illicit drug use is an increasingly important predisposing factor to ascertain during the initial evaluation. The differential diagnosis of chest pain as a result of aortic dissection includes diagnoses such as myocardial ischemia, aortic aneurysm, acute aortic regurgitation, pericarditis, musculoskeletal pain, and pulmonary embolus. It is essential to consider aortic dissection in each case as specific therapy (e.g., thrombolytic therapy for acute myocardial infarction) may impact the survivability of acute dissection.

Patients suffering acute dissection appear ill. Tachycardia is usually accompanied by hypertension in the setting of baseline essential hypertension and increased catecholamine levels from pain and anxiety. Hypotension and tachycardia may result from aortic rupture, pericardial tamponade, acute aortic valve regurgitation, or even acute myocardial ischemia with involvement of the coronary ostia. An abnormal peripheral vascular examination is present in less than 20% to 40% of patients with acute aortic dissection but when present may indicate the type of dissection. Absence of pulses in the upper extremity suggests ascending aortic involvement, whereas pulse deficits in the lower extremities speak to involvement of the distal aorta. These findings are subject to change as the dissection progresses or reentry into the true lumen occurs. Auscultation of the heart may reveal a diastolic murmur consistent with acute aortic regurgitation or an S3 indicating left heart volume overload. Physical exam findings such as jugular venous distension and a pulsus paradoxus are signs of pericardial tamponade that should be identified in any unstable patient to initiate the correct diagnostic and treatment algorithms. Unilateral loss of breath sounds, usually the left, may indicate hemothorax as a result of aortic leak or rupture with hemothorax. Alternatively, a pleural effusion may exist secondary to pleural inflammation related to the dissection. This finding requires additional evaluation prior to treatment.

A complete central and peripheral neurologic exam is critical in that abnormalities are present in up to 40% of acute type A dissections. Involvement of the brachiocephalic vessels with loss of brain perfusion may result in transient syncope or stroke. Syncope may also result from rupture into the pericardium and is an ominous sign. Stroke rarely improves with restoration of blood flow and may even cause hemorrhage and brain death, yet surgery is indicated in such patients. Fortunately, stroke is a presenting feature in fewer than 5% of patients with acute type A dissection. Loss of perfusion to intercostal or lumbar arteries may result in spinal cord ischemia and paraplegia. Peripheral nerve ischemia as a result of malperfusion may yield findings similar to spinal cord malperfusion and should be discerned as these patients often improve with restoration of blood flow. Acute aortic dissection may also cause superior vena cava syndrome, vocal cord paralysis, hematemesis, Horners syndrome, hemoptysis, and airway compression as a result of local compression and mass effect.

DIAGNOSTIC STUDIES

Routine diagnostic studies including blood tests, chest x-ray, and ECG should be obtained but are often not sufficient to establish the diagnosis of acute aortic dissection. Electrocardiogram often reveals no ischemic changes. Obvious ischemic changes are present in up to 20% of acute type A dissections, while only nonspecific repolarization abnormalities are present in nearly one third of patients with coronary ostial involvement. The ECG may also reveal left ventricular hypertrophy in those patients with long-standing hypertension. The chest x-ray is abnormal in 60% to 90% of patients with acute dissection (Fig. 45-4). Although most patients have at least one, if not several abnormal findings, a normal chest x-ray does not rule out the diagnosis. Blood should be drawn and sent for complete blood count, serum electrolytes, creatine kinase with myocardial isoenzymes, and troponin, and a blood type and screen are obtained. These tests obtained at the time of initial observation are usually unremarkable. There is frequently a mild to moderate leukocytosis. Anemia may result from sequestration of blood or hemolysis. Liver function tests, serum creatinine, myoglobin, and lactic acid may all be abnormal in the setting of certain malperfusion syndromes depending on duration.



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FIGURE 45-4 Plain chest x-ray exhibiting many features of acute type A dissection such as a widened mediastinum, rightward tracheal displacement, irregular aortic contour with loss of the aortic knob, an indistinct aortopulmonary window, and a left pleural effusion.

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DIAGNOSTIC IMAGING

Diagnostic imaging is essential to classify acute aortic dissection, regardless of the clinical certainty with which the diagnosis is made or the acuity of the patient. The diagnosis should be made rapidly and with minimal distress for the patient. Two imaging modalities currently meet these criteria and are used to diagnose acute aortic dissection: computerized tomography and echocardiography. Magnetic resonance imaging and aortography, with or without intravascular ultrasound, are used to diagnose acute aortic dissection but are second-line modalities for various reasons. The benefits, disadvantages, and diagnostic accuracy of each are useful when choosing the most appropriate study for a particular clinical situation (Table 45-3). Each test provides unique information, which may include the site of intimal disruption, reentry points, whether there is flow or thrombus in the false lumen, status of the aortic valve, presence and nature of myocardial ischemia, and brachiocephalic and aortic branch vessel involvement. Specific data may be necessary for operative planning and subsequent management to define the imaging study most appropriate for a particular patient.


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TABLE 45-3 Sensitivity and specificity of various imaging modalities useful for the diagnosis of thoracic aortic dissection

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Helical computerized tomography scanning (CT) is widely available and now the most frequently utilized test to diagnose acute aortic dissection. It requires intravenous contrast medium that may limit its use in certain clinical situations but generates images familiar to most practitioners and has a high sensitivity and specificity. This technique can be performed quickly fulfilling the requirements for use in the early management of acute dissection. Additional structures such as the pleural and pericardial spaces are imaged. When performed and formatted as an arteriogram, aortic branch vessels may also be evaluated; involvement of the brachiocephalic vessels is identified with nearly 96% accuracy. The diagnosis of dissection requires two or more channels separated by a dissection flap (Fig. 45-5). Transaxial two-dimensional images can be reconstructed to display three-dimensional images of the aorta that not only aid in diagnosis but also are useful for operative planning.



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FIGURE 45-5 Axial image of CT arteriogram of acute type A dissection showing a dissection flap in the mid-ascending aorta.

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Transesophageal echocardiography (TEE) is currently the second most frequently utilized study for making the diagnosis of acute aortic dissection. It is widely available, requires no intravenous contrast or radiation, and generates dynamic images of the aorta from which the diagnosis can be made (Fig. 45-6). It requires operator expertise both to acquire the necessary images and to conduct of the examination safely. Although the safest setting in which to perform TEE is the operating room under general anesthesia, it can be performed in a monitored setting using topical anesthesia and light sedation. Patient comfort is paramount in this situation as rupture has been reported during difficult studies and a complete examination of the entire aorta is necessary to exclude the diagnosis of acute dissection. Absolute contraindications to TEE include esophageal abnormalities such as varices, stricture, or tumor. A full stomach or recent meal are relative contraindications, but recognition of these conditions permits safe examination with few complications in the vast majority of patients. Criteria for making the diagnosis of acute aortic dissection include visualization of an echogenic surface separating two distinct lumens, repeatedly, in more than one view, and which can be differentiated from normal surrounding cardiac structures. The true lumen is identified by expansion during systole and collapse in diastole. Communication of the false lumen is found by identifying distal tears in the flap and flow in the false lumen with the addition of color Doppler; similarly, the absence of flow indicates false lumen thrombosis. TEE additionally may provide high-quality images of the aortic valve and pericardial space. The coronary ostia are directly evaluated and regional left ventricular function may be assessed to identify myocardial ischemia indirectly. Color flow Doppler reliably quantifies aortic regurgitation and may be used to assess for additional valvular abnormalities. The pericardium and pleural space are also visualized and therefore effusions may be identi-fied.



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FIGURE 45-6 Transesophageal echocardiogram showing the dissection membrane (arrows) in the short (left panel) and long (right panel) views of a type A dissection.

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Transthoracic echocardiography provides images of the ascending aorta and sections of the aortic arch that may yield the diagnosis but with much less sensitivity than transesophageal imaging. As such, transthoracic imaging may prove useful but is generally insufficient to reliably establish the diagnosis. Transthoracic evaluation is additionally limited by patient-related factors including body habitus, emphysema, and mechanical ventilation. A negative transthoracic study should be complemented by a transesophageal study, which provides greater detail of the entire aorta.

Aortography was the first study used to diagnose acute dissection in 1939 and until recently was considered the gold standard for diagnosis. It is an invasive test requiring nephrotoxic contrast media in which the aorta is visualized in multiple two-dimensional projections. The diagnosis of dissection depends upon visualization of the intimal flap, two distinct lumens, or compression of the true lumen by flow through an adjacent false lumen (Fig. 45-7). Indirect signs of dissection include the presence of branch vessel abnormalities and abnormal intimal contour on injection of the false lumen. The status of the aortic valve may be evaluated and coronary angiography in the setting of type A dissections is possible only with this diagnostic test. Coronary angiography is, however, not recommended given that the coronary ostia are involved in 10% to 20% of acute type A dissections and are easily evaluated at the time of surgery. Coronary atherosclerosis is present in 25% of all patients with acute aortic dissection, but even in those patients repair of the dissection should take precedence. Aortography is sometimes useful in acute type B dissections with evidence of mesenteric ischemia or oliguria and in type A dissection with signs of malperfusion because catheter-based intervention may be possible. Aortography may yield false-negative results with thrombosis of one lumen or when contrast equally opacifies each lumen, impairing distinction of a separate true and false lumen. The diagnosis of intramural hematoma may also be difficult given the absence of intimal disruption, while penetrating atherosclerotic ulcer is usually easily visualized. Visualization of the dissection variants is best with either CT scanning or MRI (Figs. 45-8 and 45-9). One major limitation to the use of aortography in the acute setting is the need for skilled personnel. The time required to assemble this team varies with each institution, rendering aortography less useful when compared to other immediately available diagnostic tests. Aortography also requires arterial access, which can be painful and precipitate rupture or dissection extension.



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FIGURE 45-7 Aortogram of acute type B dissection illustrating differential contrast enhancement of the true and false lumens in the descending thoracic aorta. The intimal flap (arrowhead) can be seen separating the two lumens.

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FIGURE 45-8 Axial image from CT arteriogram showing an intramural hematoma of the descending thoracic aorta (arrowhead).

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FIGURE 45-9 Sagittal contrast-enhanced MRI of penetrating atherosclerotic ulcer of the ascending aorta (arrowhead).

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Intravascular ultrasound is a catheter-based imaging tool that provides dynamic imaging of the aortic wall and an intimal flap in patients with aortic dissection. It is particularly useful in delineating the proximal and distal extent of dissection and for identifying the true and false lumens in questionable cases during aortography. High-resolution images of the normal three-layered aortic wall are differentiated to identify the abnormally thin wall adjacent to the false lumen. Because the aortic wall itself is imaged, intramural hematoma and penetrating atherosclerotic ulcers may also be identified. Currently, as an isolated imaging study, it is time consuming and requires skilled personnel, as with aortography, and generally is not useful as an initial study in the acute setting. It may be most useful in combination with aortography when the initial imaging studies are negative yet there remains a high clinical suspicion of dissection.

Magnetic resonance imaging (MRI) and the newer contrast-enhanced magnetic resonance angiography generate superior images reliably demonstrating aortic dissection (Fig. 45-10). In fact, some consider this the "gold-standard" imaging study given the published diagnostic accuracy. Dissection is identified as an intralumenal membrane separating two or more channels (Fig. 45-11). MRI provides detailed images of the entire aorta, the pericardium, and pleural spaces similar to those obtained with CT. Cine imaging may also be used to evaluate left ventricular function, the status of the aortic valve, and flow in aortic branch vessels as well as flow in the false lumen. It is, however, not widely available and the presence of ferromagnetic metal contraindicates its use. Another disadvantage of MRI is that artifact is identified in up to 64% of studies, which underscores the need for expert radiologic interpretation of the images. These factors account for its infrequent use in the acute setting.



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FIGURE 45-10 Sagittal contrast-enhanced magnetic resonance image of chronic type B dissection. The dissection flap (arrowhead) is clearly identified and the false lumen appears to extend the entire length of the thoracic and abdominal aorta (darker posterior lumen).

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FIGURE 45-11 Axial (A) and sagittal (B) contrast-enhanced magnetic resonance images of a chronic type A dissection.

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DIAGNOSTIC STRATEGY

The evaluation of suspected acute aortic dissection begins with a determination of the clinical likelihood that the diagnosis is correct and an evaluation of the hemodynamic stability of the patient. The unstable patient should undergo ECG to rule out acute coronary syndrome and be transferred immediately to the operating room. Medical management may be initiated as soon as the diagnosis is suspected. It is our practice to intubate and mechanically ventilate such patients while essential monitoring lines are placed. A transesophageal echocardiogram is then performed. If TEE fails to reveal acute aortic dissection, a hemodynamically unstable patient will then have a protected airway and invasive monitoring lines for subsequent evaluation of alternative diagnoses and continued resuscitation. If, however, acute dissection is suspected despite a negative TEE, CT arteriogram or aortography (potentially with intravascular ultrasound) is the next study of choice.

Clinically and hemodynamically stable patients permit a more detailed history and physical examination with imaging decisions tailored to specific aspects of the presentation. At the University of Virginia, such patients are first evaluated with a CT arteriogram. A CT scanner is located in the emergency room and these data may be obtained in less than 15 minutes. If that study is negative yet the diagnosis still entertained, transesophageal echocardiography is performed. In a recent review, an average of 1.8 imaging studies was used to correctly diagnose acute aortic dissection.12 Although TTE is a relatively insensitive study (especially in the descending thoracic aorta), patients with suspected acute type A dissection may first undergo that study. If positive, subsequent confirmation using TEE may be performed in the operating room to expedite surgical management; if negative, either CT scanning or TEE performed in the ICU is appropriate.

Natural History

Fifty percent of patients suffering acute type A aortic dissection are dead within 48 hours.16 A conventional wisdom has evolved that acute type A dissection carries a "1% per hour" mortality. Newer data, however, reveal a different prognosis such that medical management may be considered in certain high-risk groups. In one such study, type A dissection was managed medically in 28% of patients for various reasons with a 58% in-hospital mortality.17 Regardless, this relatively high mortality demonstrates that patients surviving acute type A dissection must be quickly and aggressively diagnosed and managed.

The natural history of acute type B dissection is difficult to determine primarily because early autopsy series failed to analyze these patients as a distinct group. As a result, most of the studies estimate a 50% mortality for untreated acute type B dissection. More contemporary data from Elefteriades et al, however, reveal a 9% initial hospital mortality for acute type B dissection with 66% of the remaining patients having no specific aortic complications requiring surgery.18 These data are obviously influenced by modern medical treatment but speak to a more benign clinical course when compared to type A dissection.

Initial Medical Management

Recognizing the natural history of patients with aortic dissection dictates that management occurs as part of the initial diagnostic evaluation. The initial patient encounter therefore focuses as much on making the diagnosis as in identifying factors that require immediate treatment. The site of this initial evaluation and resuscitation is determined primarily by the hemodynamic stability of the patient. The unstable patient belongs in the operating room, whereas a more detailed diagnostic approach from which management follows on an urgent basis can be undertaken in stable patients. Therefore, the hypotensive patient who may be hypovolemic as a result of blood loss into the thorax or pericardium undergoes the aforementioned evaluation and resuscitation on transfer to the operating room. It is preferable to avoid procedures such as transesophageal echocardiography or central line placement on an awake patient outside the operating room because hypertension resulting from patient discomfort may precipitate aortic rupture or propagation of dissection.

In the stable patient, blood pressure is measured in both arms and immediately treated to achieve a target systolic blood pressure between 90 and 110 mm Hg. Blood pressure control in hypertensive patients with pain should first be treated with narcotic analgesics. In general, the goals of hypertension management in acute aortic dissection are 2-fold.8 First, aortic wall stress is lowered by decreasing the systolic blood pressure, which reduces the possibility of rupture. Second, shear stress on the aorta is decreased by minimizing the rate of rise of aortic pressure to decrease the likelihood of dissection propagation, so-called anti-impulse therapy. The drugs most commonly used for these purposes are sodium nitroprusside and esmolol. Sodium nitroprusside is a direct arterial vasodilator with a short onset and duration of action, which make it ideal to rapidly achieve the target systolic blood pressure. The rate of rise of aortic pressure, however, is increased when sodium nitroprusside is used alone. Esmolol is added to decrease the inotropic state of the myocardium and to decrease the heart rate. This drug is a beta-1 selective blocking agent with a short half-life that can easily be titrated to achieve the target blood pressure. Loading doses for esmolol and sodium nitroprusside should be avoided to prevent hypotension. Alternative beta-1 blocking drugs such as propranolol or metoprolol, and the combined alpha and beta blocker labetolol are appropriate in the subacute phase. Alternatively, calcium channel blockers may be necessary to reduce systolic blood pressure in those patients with a contraindication to beta-blocker use. There are, however, no compelling data supporting their efficacy in acute dissection.

Operative Indications

The goals of surgery in acute type A dissection are to prevent aortic rupture into the pericardium or pleural space and to avoid involvement of the coronary ostia or aortic valve (Table 45-4). The presence of ascending aortic involvement is, therefore, an indication for operative management in all but the highest-risk patients. The difficulty arises in determining which patients are high risk and which additional factors should affect the management algorithm. Patient age, for example, is not regarded as an absolute contraindication to surgery. This fact should perhaps be considered, however, given the few reported survivors of operative treatment for acute type A dissection greater than 80 years of age. Neurologic status at the time of presentation can also affect the decision to operate. While most agree that obtunded or comatose patients are unlikely to improve with surgical repair, complications such as stroke or paraplegia at the time of presentation are not contraindications to surgical correction. The status of the dissection should not be a factor; thrombosis of either lumen occurs but these patients remain at risk for lethal complications and surgery is indicated. Similarly, patients with subacute type A dissection who present or are referred longer than 2 weeks following the event require operation. Scholl et al demonstrated that these patients have avoided the early complications of dissection and may safely undergo elective operation rather than emergency repair.19


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TABLE 45-4 Operative indications for acute and chronic type A and B thoracic aortic dissections

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The goals of surgical management of complicated acute type B dissection are the prevention of free rupture and perfusion of end organs in the absence of symptoms. The most frequent causes of death in acute type B dissection are aortic rupture and visceral malperfusion. These, however, occur much less frequently with medical management than do complications of acute type A dissection treated nonoperatively. Between 70% and 80% of patients with acute type B dissection survive the acute and subacute phases with medical management alone. Such success with medical management has traditionally relegated surgical treatment for acute type B dissections to the complications of medical management or progression of disease (see Table 45-4). The indications for repair include contained or free aortic rupture, acute aortic expansion, malperfusion syndrome, pain or progression of dissection despite maximal medical management, and failure of medical management to control hypertension. Although medical management of acute type B dissection is the rule in most centers, some centers advocate immediate surgical intervention in selected patients with uncomplicated acute type B dissection. Factors which may favor early operation in acute type B dissection are the presence of Marfan syndrome, a large false aneurysm, arch involvement, and presumed medical compliance issues.20 As in acute type A dissection, acute paralysis does not contraindicate surgery because patients can have remarkable improvement following revascularization.

There is some debate regarding the treatment of patients diagnosed with intramural hematoma and penetrating atherosclerotic ulcer. Recent data regarding the natural history of these dissection variants have made the issue less confusing. Intramural hematoma may lead to acute rupture in up to 35% of patients, whereas regression or no change in the hematoma is seen in the majority of medically managed patients surviving the initial period. Similarly, patients with penetrating atherosclerotic ulcer were found to have a 42% rate of acute rupture.21 As a result of these relatively high acute rupture rates, the Yale group currently recommends early operative intervention for intramural hematoma and penetrating ulcer involving the ascending aorta. In the descending aorta, medical management with anti-impulse therapy and a low threshold for operative intervention result in the lowest mortality. These patients require continuous observation and repeat diagnostic imaging after 3 to 5 days in the hospital to monitor the lesion.

Operative Technique

ANESTHESIA AND MONITORING

Anesthesia used during the repair of aortic dissections is often narcotic-based with inhalational agents for maintenance. Single-lumen endotracheal tubes are used for procedures performed through a median sternotomy while double-lumen endotracheal tubes are useful but not mandatory for procedures performed through a left thoracotomy. Monitoring lines often include central venous access with a pulmonary artery catheter and one or more arterial pressure monitoring lines specific to the operation performed. One or two radial arterial lines and at least one femoral line are required to ensure adequate perfusion of the upper and lower body. All patients require a transesophageal echocardiography probe for various reasons. Core body temperature is monitored in the bladder using a Foley catheter and in the esophagus using a nasopharangeal probe. A wide skin preparation to include the axillary and femoral arteries is essential to provide all possible cannulation options.

HEMOSTASIS

Surgical procedures for aortic dissection can be associated with significant blood loss. Strict blood conservation is an important aspect of the operation and at least one cell-saver device should be available. Packed red blood cells, platelets, and fresh frozen plasma should be in the operating room at the start of the operation. Coagulopathy as a result of the preoperative status of the patient, cardiopulmonary bypass, and deep hypothermic circulatory arrest contribute to excessive blood loss. Improvements in vascular graft material have all but eliminated this as a reason for intra- and postoperative blood loss. Antifibrinolytic drugs such as epsilon-aminocaproic acid and aprotinin are useful hemostatic adjuncts. Aprotinin is particularly useful when used in either the full or one-half Hammersmith regimen and is most effective when administered prior to the operation. In cases where deep hypothermic circulatory arrest is used, aprotinin is administered in our practice only after the period of circulatory arrest. Patients will often require transfusion of fresh frozen plasma, platelets, and possibly cryoprecipitate. Fibrin glues and hemostatic materials such as Surgicel and Gelfoam are useful as systemic coagulopathy is corrected.

CARDIOPULMONARY BYPASS

There are various options for arterial and venous cannulation sites based upon the type of dissection. Arterial cannulation of the uninvolved distal aortic arch is preferable in acute type A dissection. Cannulation of the true lumen of the dissected ascending aorta is possible and can be accomplished quite easily using the Seldinger technique over a long wire introduced and guided by transesophageal echocardiography. Alternative sites include the right subclavian and the innominate artery for antegrade perfusion, or either femoral artery with retrograde aortic perfusion. In any case of retrograde aortic perfusion, it is essential to monitor proximal perfusion with a functioning radial arterial catheter.

There is debate over which femoral artery to cannulate in the setting of lower extremity malperfusion with a pulse deficit. Dissection of the abdominal aorta often leaves the left femoral artery originating from the false lumen and therefore cannulation of the right femoral artery will most often perfuse the true lumen. Perfusion of the false lumen can cause retrograde dissection and malperfusion of aortic branch vessels arising from the true lumen. In that event, cardiopulmonary bypass should be stopped for aortic cannulation through an alternative site to achieve whole body perfusion. If the chest has been opened, direct cannulation of the ascending aorta is often successful when guided by transesophageal echocardiography. An alternative cannulation technique is through the left ventricular apex and aortic valve. The cannula is then held in position with an ascending aortic tourniquet. Fortunately, there are usually multiple reentry tears throughout the dissection flap which permit perfusion of both lumen regardless of the lumen cannulated.

Venous cannulation is most often through the right atrium using a two-stage venous cannula, while bicaval cannulation is reserved for certain cases in which retrograde cerebral perfusion is preferred during circulatory arrest. A left ventricular vent is necessary in the setting of aortic valve incompetence and is easily placed through the right superior pulmonary vein or rarely through the left ventricular apex wall. Cardioplegia is administered retrograde through a coronary sinus catheter with additional protection via direct cannulation of the undissected coronary ostia.

The formerly popular "clamp and sew" technique used for repair of acute type B dissection has largely been replaced by the use of partial left heart bypass. Arterial cannulation sites for this technique include the distal thoracic aorta for limited dissections of the proximal descending thoracic aorta or the femoral artery for those extending into the abdomen. Venous drainage of oxygenated blood is through the left inferior pulmonary vein or the left atrium via the appendage when accessible. This technique does not require an oxygenator or pump suction and therefore the dose of heparin (100 U/kg) is less than with full cardiopulmonary bypass.

CEREBRAL PROTECTION

Surgical repair of aortic dissection involving the arch requires disruption of adequate blood flow to the brain during a period of circulatory arrest. Cerebral protection during that period is paramount and may be achieved through either deep hypothermia with cessation of electrical activity or some form of continued cerebral perfusion. Deep hypothermia during circulatory arrest was the first method used to perform operations on the aortic arch and remains an effective method for shorter procedures. Generally, periods of circulatory arrest up to 14 minutes are acceptable at 25?C, and periods up to 31 minutes appear to result in only transient neurologic sequelae at 15?C in a small number of patients.22 Specifically, the risk of transient neurologic dysfunction on cognitive testing following a period of circulatory arrest is roughly 10% at less than 30 minutes, but increases to 15% at 40 minutes, 30% at 50 minutes, and 60% at 60 minutes.23

It is critical to correctly estimate brain temperature for expected outcome. Nasopharyngeal and tympanic temperatures are measured to estimate brain temperature but are imperfect. For that reason, some groups use electroencephalographic silence to determine the appropriate point at which to discontinue cooling and perfusion. Slow systemic cooling on cardiopulmonary bypass (2025 minutes) while maintaining a maximal temperature gradient between perfusate and patient of less than 10?C is ideal. The head is then packed in ice to maintain a low brain temperature. While cooler temperatures increase the safe interval of circulatory arrest, cooling to lower than 15?C may result in a form of nonischemic brain injury and is therefore not recommended. Methylprednisolone and thiopental administration during cooling are adjunctive measures thought by some to decrease cerebral metabolic requirements during the period of circulatory arrest, but we currently do not use either. Reinstitution of cardiopulmonary bypass with systemic rewarming following repair proceeds without exceeding a 10?C temperature gradient to at least 37?C as core body temperature often falls briefly after cessation of active warming and separation from cardiopulmonary bypass. Furosemide and mannitol are administered to initiate diuresis and to promote free radical scavenging following circulatory arrest.

Continued cerebral perfusion during the period of circulatory arrest is an alternative technique for cerebral protection. Cerebral blood flow may be delivered in either a retrograde or antegrade fashion. The technique for retrograde cerebral perfusion depends upon the venous cannulation strategy. If bicaval cannulation is required, reversing flow through the superior vena caval cannula with a proximally placed tourniquet is simple and effective. Dual-stage venous cannulation requires placement of a retrograde coronary sinus catheter into the superior vena cava through a purse-string suture. Retrograde cerebral perfusion has the added benefit of flushing atherosclerotic material and air from the brachiocephalic vessels. A flow rate necessary to produce a superior vena caval pressure of 15 to 25 mm Hg is considered optimal. Selective antegrade cerebral perfusion has recently gained popularity. Once the aortic arch is open, the innominate artery and the left common carotid artery are encircled with vessel occluders and each lumen cannulated with a retrograde coronary sinus cannula. With the left subclavian artery occluded, flow rates are slowly increased to achieve perfusion pressures of 50 to 70 mm Hg at the desired circulatory arrest temperature. These cannulae are then removed just prior to completing the anastomosis of the brachiocephalic vessels to the vascular graft, at which time cardiopulmonary bypass may be reinstituted.

TECHNIQUES FOR TYPE A DISSECTION

The exposure for procedures performed on the ascending aorta and the proximal arch is through a median sternotomy. This can be modified with supraclavicular, cervical, or trapdoor incisions to gain exposure to brachiocephalic vessels or the descending thoracic aorta. When dissecting the distal arch, it is important to identify and protect both the left vagus nerve with its recurrent branch and the left phrenic nerve. Replacement of the ascending aorta in type A dissections is best performed by an open distal anastomosis technique if the arch is involved (30%) or if arch involvement is unknown. The open distal anastomotic technique requires clamping the mid ascending aorta and cardiac arrest via administration of antegrade and/or retrograde cardioplegic solution. The dissected ascending aorta proximal to the clamp is then opened. Evaluation and surgical correction of the aortic valve is ideally performed at this time while systemic cooling continues. If dissection does not involve the aortic root, the aorta is transected 5 to 10 mm distal to the sinotubular ridge. If dissection involves the sinotubular ridge, the proximal aorta is reconstructed by reuniting the dissected aortic layers between one or two strips of Teflon felt using either 3.0 or 4.0 Prolene suture. Safi et al use a technique of interrupted pledgeted horizontal mattress sutures as compared to the felt sandwich technique. In their experience, this provides superior stabilization and decreases the potential for subsequent aortic stenosis. There has also been a great deal of enthusiasm for reuniting the dissected layers using gelatin-resorcinol-formalin (GRF) glue or the newer BioGlue (Cryolife International Inc., Kennesaw, GA). There are, however, concerns regarding each of the commercially available types of glue in that redissection and toxicity from constituents of the glue (formalin) have been reported.

Once the temperature reaches 18?C to 20?C, perfusion is discontinued during a brief period of circulatory arrest. The aortic clamp is released and the intima of the aortic arch is inspected and repaired accordingly (Fig. 45-12). If the intima is intact, the distal anastomosis is performed and the graft is cannulated, de-aired, and clamped for resumption of cardiopulmonary bypass with systemic warming. If the intima of the arch is violated, then a hemiarch reconstruction is performed (Fig. 45-13). We have only rarely found it necessary to perform a complete arch resection for an acute dissection. If a complex aortic root procedure is required, it is often useful to repair the aortic root with one vascular graft and use a separate graft to create the distal aortic anastomosis. The two grafts are then measured, cut, and anastomosed to provide the correct length and orientation for aortic replacement.



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FIGURE 45-12 The false lumen of the distal aorta is closed and the aortic wall is reconstructed with inside and outside felt strips. (Reproduced with permission from Stone C, Borst H: Dissecting aortic aneurysm, in Edmunds LJ Jr (ed): Cardiac Surgery in the Adult. New York, McGraw-Hill, 1997; p 1125.)

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FIGURE 45-13 (A) The type A dissection extends into the proximal aortic arch. (B) The distal dissected aortic wall is reconstructed with inside and outside felt strips to replace part of the arch and ascending aorta. (Reproduced with permission from Stone C, Borst H: Dissecting aortic aneurysm, in Edmunds LJ Jr (ed): Cardiac Surgery in the Adult. New York, McGraw-Hill, 1997; p 1125.)

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If the ascending aorta cannot be cross-clamped, the patient is cooled to 20?C with subsequent circulatory arrest. The distal aortic reconstruction is performed first in this circumstance, at which time the graft is cannulated and proximally clamped with resumption of cardiopulmonary bypass and systemic rewarming. Cannulation of the graft for antegrade systemic perfusion and rewarming is associated with improved neurologic outcome compared to retrograde perfusion and should be performed whenever possible. Newly available vascular grafts include 7- to 8-mm Dacron side-arm grafts for easy cannulation to facilitate this technique. Because a cross-clamp is not applied, the left ventricle must be decompressed once fibrillation starts during systemic cooling (approximately 20?C) to prevent distension and irreversible myocardial injury. Proximal ascending aortic repair is completed during the period of rewarming.

An alternative to the open distal technique is possible when dissection is limited to the ascending aorta or the proximal arch away from the origin of the brachiocephalic vessels. Antegrade arterial perfusion is achieved through distal arch or right subclavian artery cannulation; retrograde perfusion via cannulation of a femoral artery has traditionally provided acceptable results. An aortic cross-clamp is applied tangentially just proximal to the innominate artery. The ascending aorta is resected to include the inferior aspect of the arch. The layers of the dissected aorta proximal to the clamp are then reunited if necessary and the ascending aorta replaced with an appropriately sized, beveled vascular graft. The proximal reconstruction and anastomosis may then be performed and the entire procedure performed without requiring deep hypothermia and circulatory arrest.

Isolated dissection of the aortic arch is rare. Classified as a type A dissection, it requires resection of the arch at the site of intimal disruption and aortic replacement. Surgical management of the brachiocephalic vessels is determined by the integrity of the adjacent intima. If intact, the brachiocephalic vessels are reimplanted as a Carrel patch into a vascular graft after repair (Fig. 45-14). If the dissection involves individual vessels, each may require repair and reimplantation individually into the graft used for arch replacement (Fig. 45-15).



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FIGURE 45-14 Brachiocephalic vessels can be reattached to an arch graft as a unit if the inner cylinder of origin of each vessel remains intact. (A) The arch vessels are excised as a unit from the superior surface of the dissected aortic arch. (B) The separated layers of the brachiocephalic patch are reunited using inner and outer felt strips and continuous suture. (C) A corresponding hole is cut into the aortic graft and the brachiocephalic unit is sutured into place. (Reproduced with permission from Stone C, Borst H: Dissecting aortic aneurysm, in Edmunds LJ Jr (ed): Cardiac Surgery in the Adult. New York, McGraw-Hill, 1997; p 1125.)

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FIGURE 45-15 The brachiocephalic vessels are separated from the true lumen by the dissected false lumen (left panel). If individual brachiocephalic vessels also are damaged beyond repair, short, interposition grafts are added to reconnect each artery to the aortic graft (right panel). (Reproduced with permission from Stone C, Borst H: Dissecting aortic aneurysm, in Edmunds LJ Jr (ed): Cardiac Surgery in the Adult. New York, McGraw-Hill, 1997; p 1125.)

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Aortic root dissection often fails to violate the intima of the coronary ostia. Repair of the ascending aorta at the sinotubular junction is therefore sufficient to reunite the aortic root layers and provide uninterrupted coronary blood flow. Minimal disruption of the coronary ostial intima should be repaired primarily with 5-0 or 6-0 Prolene suture. If, however, the ostium is circumferentially dissected and an aortic root replacement is necessary, an aortic button should be excised and the layers reunited with running 5-0 Prolene suture, glue, or both. Coronary buttons are then reimplanted into the vascular graft or to a separate 8-mm vascular graft as part of a Cabrol repair (Fig. 45-16). Aortocoronary bypass grafting is performed only when the coronary ostium is not reconstructable and as a last resort.



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FIGURE 45-16 llustration showing attachment of the coronary ostia to the graft using the Cabrol technique. The ends of a 60-mm Dacron graft are sewn end-to-end to each coronary ostium. A side-to-side anastomosis is made between the intercoronary tube graft and the aortic graft. (Reproduced with permission from Stone C, Borst H: Dissecting aortic aneurysm, in Edmunds LJ Jr (ed): Cardiac Surgery in the Adult. New York, McGraw-Hill, 1997; p 1125.)

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Acute type A dissection is complicated by aortic valve insufficiency in up to 75% of patients. Fortunately, preservation of the native valve is successful nearly 85% of the time. The mechanism of aortic insufficiency in most cases is the loss of commissural support of the valve leaflets. This is repaired using pledgeted 4-0 Prolene sutures to reposition each of the commissures at the sinotubular ridge (Fig. 45-17). The dissected aortic root layers are then reunited using 3-0 Prolene suture and either one or two strips of Teflon felt. Bioglue is placed between the layers prior to suture repair of the sinotubular ridge to buttress the repair and reform the sinuses of Valsalva. Aortic valve preservation must always be performed using intraoperative transesophageal echocardiography to assess the valve postoperatively. No more than mild aortic insufficiency should be present. In addition to commissural resuspension, techniques exist to spare the aortic valve and replace the aortic root in acute type A dissection, but the experience is early and the number of patients few. This topic is covered in greater detail in the section on surgical techniques for chronic type A dissection.



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FIGURE 45-17 Resuspension and preservation of the native aortic valve in a type A dissection. The dissected layers are approximated at each commissure with double pledgeted mattress sutures. Completed resuspension of the aortic valve commissures. Thin felt strips (810 mm wide) are placed inside and outside around the circumference of the aorta. The coronary ostia are not compromised. The aortic walls are sandwiched between the felt strips with horizontal mattress sutures. A vascular graft is sutured to the reconstructed proximal aorta. (Reproduced with permission from Stone C, Borst H: Dissecting aortic aneurysm, in Edmunds LJ Jr (ed): Cardiac Surgery in the Adult. New York, McGraw-Hill, 1997; p 1125.)

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If the aortic valve cannot be spared, replacement of the ascending aorta and valve should be performed using a composite valve graft or homograft. The composite valve graft is implanted using horizontal mattress 2-0 Tycron sutures to encircle the annulus and to seat the valved conduit (Fig. 45-18). The previously excised and reconstituted coronary buttons are reimplanted into the vascular graft with running 5-0 Prolene suture (Fig. 45-19). The left coronary button is implanted first, at which time the graft is clamped and placed under pressure to define the proper orientation and position of the right coronary button. The aortic homograft is similarly implanted using horizontal mattress 2.0 Tycron sutures, except that a generous margin of aortic root below the coronary buttons is retained for a second hemostatic suture line of running 4-0 Prolene. This is an ideal solution for individuals who have a contraindication to anticoagulation or for young females. The Ross procedure (pulmonary autograft) is not applicable in those patients with connective tissue disorders and not recommended in acute dissection.



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FIGURE 45-18 Everting 2-0 pledgeted mattress sutures are placed shoulder-to-shoulder around the aortic annulus to anchor a composite graft containing a St. Jude prosthesis. (Reproduced with permission from Stone C, Borst H: Dissecting aortic aneurysm, in Edmunds LJ Jr (ed): Cardiac Surgery in the Adult. New York, McGraw-Hill, 1997; p 1125.)

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FIGURE 45-19 The coronary ostia are attached to the graft by the button technique using a continuous 5-0 Prolene suture. (Reproduced with permission from Stone C, Borst H: Dissecting aortic aneurysm, in Edmunds LJ Jr (ed): Cardiac Surgery in the Adult. New York, McGraw-Hill, 1997; p 1125.)

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Endovascular stent grafting is currently under investigation as a definitive form of management in acute type B dissection and in conjunction with surgery for acute type A dissection. Long-term data and prospective comparisons to surgery will be necessary before percutaneous management can be recommended as an alternative to surgery.

TECHNIQUES FOR TYPE B DISSECTION

The right lateral decubitus position is optimal for surgical treatment of acute type B dissections requiring operation. The pelvis is canted posteriorly to allow access to both sets of femoral vessels. A posterolateral thoracotomy in the 4th intercostal space provides sufficient access to the aorta; notching the 5th and 6th ribs posteriorly permits visualization of the entire thoracic aorta distally. A thoracoabdominal incision may be required to access the abdominal aorta in the case of visceral malperfusion. This may be performed either through the abdomen or the retroperitoneum. The left hemidiaphragm must be carefully divided in a radial fashion while marking adjacent sites on each side of the division with metal clips. This provides all necessary exposure and facilitates subsequent diaphragm approximation at the end of the case.

The ideal operation for acute type B dissection is replacement of as little of the descending thoracic aorta as is necessary. The extent of replacement rarely exceeds the proximal third and includes the primary tear in most cases. Such a strategy optimizes preservation of intercostal arteries perfusing the spinal cord to combat an incidence of paraplegia that may be as high as 19% following surgery for acute type B dissections.24 This point is controversial, however, and some groups advocate replacement of the entire thoracic aorta. Any less extensive aortic replacement leaves dissected aorta with the potential for late aneurysmal dilatation when there is perfusion of the false lumen. The ideal strategy to minimize spinal cord malperfusion yet resect all involved aorta has not been devised.

Once the thoracic aorta has been exposed, the operation continues with division of the mediastinum between the left subclavian and the left common carotid arteries. The left subclavian artery is encircled with an umbilical tape and Rommell tourniquet. It is essential that the left vagus and recurrent laryngeal nerves are identified and preserved during the course of the dissection. Ultimately, the entire distal arch must be free enough to place an aortic clamp between the left common carotid and left subclavian arteries. Next, the proximal descending thoracic aorta is circumferentially mobilized, dividing intercostal arteries in the segment to be excised. The left inferior pulmonary vein is then dissected and a 4-0 Prolene purse-string suture placed posteriorly to cannulate for partial left heart bypass. Following the administration of 100 U/kg of intravenous heparin, 14F cannulae are inserted into the left inferior pulmonary vein and either a normal appearing area of descending thoracic aorta or percutaneously into either femoral artery. Bypass is then initiated with flow rates between 1 and 2 L/min. The left subclavian artery is controlled and vascular clamps are placed on the aorta proximally and distally on the mid-thoracic aorta. Right radial artery pressure is measured to maintain proximal aortic systolic pressure between 100 and 140 mm Hg and mean femoral artery pressure greater than 60 mm Hg.25 The aorta is then opened longitudinally and bleeding from intercostal arteries is controlled by suture ligation. Transection of the aorta distal to the origin of the left subclavian artery provides a site for the proximal anastomosis. This is performed using 3-0 Prolene suture and may require external reinforcement with Teflon felt strips.

The graft inclusion technique is another technique in which the posterior aspect of the proximal aorta is not fully transected. The proximal anastomosis is then made to the intact posterior aspect of the aorta. We do not recommend this technique since one cannot be certain of anastomosing all layers of the aorta. The size of the vascular graft is based on the diameter of the distal aorta and beveled to match the aorta proximally. This anastomosis may include the origin of the left subclavian to treat dissection in this vessel. A separate 6- to 8-mm Dacron graft can be used if there is intimal disruption involving the proximal segment of the left subclavian artery. Once the proximal anastomosis is complete, the proximal clamp is released and repositioned on the vascular graft to inspect the anastomosis. Attention is then turned to repairing the distal aorta with Teflon felt or glue. The distal anastomosis is completed, the clamps are released, and partial left heart bypass is terminated. Decannulation is routine except that percutaneously placed femoral artery cannulae 14F or smaller may be removed without direct repair. When cannulae larger than 15F are required, open surgical repair of the femoral arteriotomy is indicated.

Acute type B dissection extending into the abdominal aorta may be approached using total cardiopulmonary bypass and deep hypothermic circulatory arrest to prevent potential cerebral, spinal cord, and intra-abdominal organ ischemia.26 After creation of a thoracoabdominal incision, the thoracic and abdominal aorta are exposed from the left subclavian artery to the aortic bifurcation. The femoral artery and vein are cannulated for cardiopulmonary bypass with systemic cooling. With the head packed in ice, cardiopulmonary bypass is then interrupted and the aorta opened proximally. The arch is repaired if necessary with Teflon felt or glue and the proximal anastomosis created. The graft is then clamped distal to the anastomosis and cannulated for proximal perfusion with resumption of cardiopulmonary bypass. Intercostal arteries to the upper third of the thoracic aorta are divided; larger vessels below T9 are reimplanted into the back of the graft with 4-0 Prolene suture. As vessels are reimplanted, the proximal clamp is moved distally to maximize spinal cord perfusion. Abdominal aortic branch vessels are divided from the wall of the aorta with a 5-mm cuff for reimplantation. Usually the right renal, superior mesenteric, and celiac arteries and adjacent intercostal and lumbar arteries are removed as a patch and reimplanted into the graft. The left renal artery often originates from a dissected segment of the aorta and is reimplanted individually after repair. The inferior mesenteric artery is often ligated as are bleeding lumbar vessels below L3. Intimal disruption of any abdominal aortic branch vessel requires repair with 5-0 Prolene suture prior to reimplantation. Once all side branches have been secured, the distal anastomosis to the aortic bifurcation is performed reuniting the aortic layers distally with Teflon felt or glue if necessary.

Rupture of the thoracic aorta prior to or during repair is a catastrophic event often leading to operative death. Successful management requires immediate cannulation of the femoral artery and vein for cardiopulmonary bypass and eventual deep hypothermic circulatory arrest, but only if the ruptured area can be locally controlled. Assisted venous drainage through the femoral vein is often adequate but direct cannulation of the right ventricle through the pulmonary artery may also be performed. A left atrial vent is placed through the left inferior pulmonary vein once the heart begins to fibrillate; the left ventricle may vented as well directly through the apex. Once the nasopharyngeal temperature reaches 15oC, the vent is occluded and cardiopulmonary bypass is stopped. The head is placed down and the aorta opened for repair under circulatory arrest. The distal aorta should be clamped to minimize blood loss. Once the proximal anastomosis is performed, the proximal clamp is moved onto the graft and the graft cannulated to resume cardiopulmonary bypass.

Spinal cord ischemia resulting in paraplegia or paraparesis is a recognized complication of acute dissection repair that may be partially preventable and even reversible. The incidence of spinal cord ischemia is between 19% and 36% following repair of acute type B dissection.24,25 Whereas various strategies exist to prevent spinal cord ischemia during repair of chronic dissection, very few are feasible in the acute setting. Pharmacologic agents such as steroids, free radical scavengers, vasodilators, and adenosine are promising adjuncts to prevent spinal cord ischemia but presently have little to no proven clinical utility. We presently use left atrial to femoral artery bypass and reimplant key intercostals arteries and selectively use cerebrospinal fluid drainage as outlined by Safi et al.27

MALPERFUSION SYNDROME

Malperfusion of aortic branch vessels may occur from the coronary ostia to the aortic bifurcation and may dominate the presentation of certain patients. Although autopsy series yield a greater percentage of patients with evidence of malperfusion, clinical series reveal that dissection is not infrequently complicated by malperfusion of at least one organ system (Table 45-5).15,28 Compression of the true lumen by the false lumen is the mechanism by which aortic branch vessel occlusion occurs in the majority of cases. Branch vessels may also be completely sheared off the true lumen and perfused to various degrees by the false lumen. Malperfusion is most often treated with primary surgical repair of the dissection, but catheter-based or open fenestration is reappearing as a potentially more effective treatment.


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TABLE 45-5 Frequency and location of malperfusion in acute type A and B thoracic aortic dissection

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Percutaneous fenestration and stenting are relatively new adjuncts to the surgical management of malperfusion syndromes. Renewed interest in these procedures grew from the recognition that hospital mortality of patients presenting with malperfusion was as high as 60%.29 Surgical fenestration to treat malperfusion, however, reduced the mortality to under 20%.30,31 Indications for percutaneous fenestration and endovascular stent placement were developed to treat malperfusion syndrome with the goal of improving outcome even further. Direct stenting of obstructed branch vessels and percutaneous fenestration with or without placement of a stent in the true lumen are the procedures most commonly performed. In certain situations, stents may be placed across an existing distal reentry tear to maintain patency and perfusion of the true lumen and the branch vessels. Balloon fenestration may be required to create such a communication between the lumen or to prevent thrombosis of the false lumen from which branch vessels may originate. Early results indicate that this procedure is both safe and effective, with restoration of flow in up to 90% of patients and an average 30-day mortality of 10% to 25%.32,33 Given that the majority of postoperative mortality in patients with acute dissection and malperfusion is related to the duration of concomitant malperfusion, one strategy is percutaneous reperfusion followed by surgical repair.34 Percutaneous treatment of malperfusion may also be performed following surgical repair of dissection but with less success in most reports.

The techniques used for surgical treatment of malperfusion depend upon location of the affected branch vessel but are generally quite similar. Malperfusion of the brachiocephalic vessels as a result of acute type A dissection is treated by repairing the dissection proximally if the intima is intact. If the intima is violated or if dissection extends into any brachiocephalic vessel, the artery should be resected from the arch, the layers reunited, and the vessel reimplanted into the arch, perhaps with an interposition vascular graft if necessary. Extra-anatomic bypass to the carotid arteries is an option in unreconstructable cases.

Malperfusion of the intra-abdominal viscera may be apparent at presentation but may also complicate surgical repair of acute type A or B dissections. Again, proximal repair of the dissection is standard treatment, but if this fails or if malperfusion persists despite repair, an additional procedure is necessary. Either open surgical or percutaneous fenestration of the dissection flap is necessary. Percutaneous fenestration is performed by pulling an inflated balloon or a fenestration knife through the dissection flap to create a communication between the two lumens. Surgical fenestration procedure is performed through a midline laparotomy or left flank incision to provide exposure of the infrarenal aorta (Fig. 45-20). Occasionally, fenestration of intra-abdominal aortic branch vessels may be required if the intima is violated beyond the ostia. If the dissection flap cannot be completely excised, the distal vessel layers must be reunited. Consideration should be given to patch angioplasty to prevent narrowing when closing smaller vessels. In the event that perfusion is not reestablished, extra-anatomic bypass may be required.



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FIGURE 45-20 Fenestration of the abdominal aorta for visceral malperfusion. A transverse incision is made into the aorta, preferably into nondissected aorta. The proximal dissection membrane is incised and then excised to decompress the false lumen as far proximally as possible. The dissected layers are reconstructed with Teflon felt or glue and the aortotomy is closed directly. (Reproduced with permission from Stone C, Borst H: Dissecting aortic aneurysm, in Edmunds LJ Jr (ed): Cardiac Surgery in the Adult. New York, McGraw-Hill, 1997; p 1125.)

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Obstruction of the terminal aorta or malperfusion of the lower extremities following operative repair is best treated with percutaneous fenestration. Surgical fenestration remains an option if percutaneous techniques fail to reestablish blood flow. In the event that surgical fenestration fails, the best solution is femoral-femoral bypass grafting in the setting of unilateral malperfusion or axillo-femoral and femoral-femoral bypass grafting if bilateral lower extremity malperfusion exists.

Postoperative Management

Invasive hemodynamic monitoring is used to ensure adequate end-organ perfusion with a target systolic blood pressure between 90 and 110 mm Hg. Early postoperative blood pressure control begins with adequate analgesia and sedation using narcotics and sedative/hypnotic agents. The patient should, however, be allowed to emerge from general anesthesia briefly for a gross neurologic examination. The patient is then sedated for a period to ensure continued hemodynamic stability and to facilitate hemostasis. Coagulopathy is aggressively treated with blood products and antifibrinolytic agents as necessary and by warming the patient. Hematocrit, platelet count, coagulation studies, and serum electrolytes are obtained and corrected as necessary. An ECG and chest radiograph are used to assess for abnormalities and to serve as baseline studies. A full physical exam including complete peripheral vascular exam is performed upon arrival. Despite adequate repair of the dissection, perfusion of the false lumen may persist and therefore malperfusion syndrome remains possible. If an abdominal malperfusion syndrome is suspected postoperatively, this should be aggressively evaluated with ultrasound and subsequent angiography if positive. A strong clinical suspicion is enough to warrant this evaluation given the consequences of failed recognition. In the morning, if the patient has been hemodynamically stable without excessive bleeding and the results of a neurologic exam are normal, the patient may be weaned from the ventilator and extubated. Management is routine from that point forward.

Long-term Management

Surviving the operation for acute dissection represents the beginning of a lifelong requirement for meticulous medical management and continued close observation. It has been estimated that replacement of the ascending aorta for type A dissection obliterates flow in the distal false lumen in fewer than 10% of patients. As a result, the natural history of repaired dissection may involve dilatation and potential rupture of the chronically dissected distal aorta. This was the reason for late death in nearly 30% of DeBakey's original series in 1982 and is currently the leading cause of late death following surgical repair.35 Often a multidrug antihypertensive regimen including beta-blocking agents is required to maintain systolic blood pressure below 120 mm Hg. There are some data indicating that blood pressure control within a narrow range may alter the natural history of chronic dissection by diminishing the rate of aneurysmal dilatation. The long-term durability of the aortic valve following supracoronary reconstruction is quite good with freedom from aortic valve replacement of 80% to 90% at 10 years. Progressive aortic insufficiency of the native valve is, however, possible and should be followed with transthoracic echocardiography in some patients.

Follow-up diagnostic imaging is required to monitor aortic diameter in patients with chronic dissection. Spiral CT arteriogram and MRI are the imaging studies of choice. MRI and ultrasound are useful in patients with renal insufficiency and in those requiring only imaging of the abdominal aorta. Echocardiography is useful for imaging the ascending aorta and provides additional information regarding the aortic valve. It is important to recognize the resolution limitations of each imaging modality and inherent imprecision of comparing different imaging modalities to evaluate changes. In general, measurements should be made at the same anatomical level with respect to reproducible anatomical structures (i.e., the sinotubular ridge, proximal to the innominate or left subclavian arteries or at the diaphragmatic hiatus). It is important to recognize that the false lumen should be included in measurements of aortic diameter whether it is perfused or not. Three-dimensional reconstruction of spiral CT and MRI scans minimizes the error introduced by aortic eccentricity when comparing imaging studies and has simplified following this patient population. The current recommendations are to obtain a baseline study prior to hospital discharge and at 6-month intervals during the first year. If the aortic diameter remains unchanged at 1 year, studies are obtained yearly. Aortic enlargement of more than 0.5 cm within a 6-month period and greater eccentricity on comparison of 3-D reconstruction images are high-risk changes for which the interval is decreased to 3 months if surgery is not indicated.

Results

The operative mortality for repair of acute aortic dissection has fallen since DeBakey's original 40% mortality was reported in 1965. Improved ICU and floor care of these patients, earlier recognition of dissection through improved imaging modalities, development of hemostatic vascular graft material, more effective hemostatic agents, and improvements in the safety of cardiopulmonary bypass are likely responsible. In the last two decades, most centers consistently report an operative mortality for acute type A dissection of around 20%. The high early mortality in acute dissection parallels the number of patients who present profoundly hypotensive and in shock. The mode of death is stroke, myocardial ischemia/heart failure, or malperfusion in most cases. The operative mortality of patients suffering acute type B dissection (28%65%) is higher than for type A dissection because the indications for surgery have traditionally been failure of medical management or complications of dissection as previously discussed.18 The most recent data from a mulitcenter international registry, however, reveal that such a disparity in operative mortality between acute type A and B dissections may be disappearing. The mortality in that study was 27% for acute type A and 29% for acute type B dissection (p = NS).36 Early death following acute dissection occurs as a result of aortic rupture or as a consequence of malperfusion.7

The published results for long-term survival following acute type A dissection surgically treated over the last decade is roughly 55% to 75% at 5 years and between 32% and 65% at 10 years.37,38 Operative repair of acute type B dissection yields 5-year survival of 48% with a 10-year survival of 29%.38


?? CHRONIC AORTIC DISSECTION
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Clinical Presentation

SIGNS AND SYMPTOMS

Chronic aortic dissection is usually asymptomatic. It may be incidentally discovered following an asymptomatic acute dissection; this most often occurs in patients with a preexisting aortic aneurysm. Some patients eventually require surgical treatment for chronic dissection and most do so as a result of aneurysmal dilatation of a chronically dissected aortic segment. Presenting complaints often include intermittent, dull chest pain or even severe skeletal pain from erosion into the bony thorax with large or rapidly expanding aneurysms. Aortic insufficiency may develop with chronic type A dissection and present with typical features of congestive failure including fatigue, dyspnea, and mild, dull chest pain. Infrequently, chronic dissection may result in paralysis/paraplegia from loss of vital intercostal arteries or even distal embolization of thrombus or atheroma from the false lumen. Malperfusion syndrome is an uncommon presentation for patients with chronic dissection given the likelihood that the true and false lumens communicate.

DIAGNOSTIC IMAGING

Diagnostic imaging of chronic aortic dissection is usually performed for surveillance but may also be necessary in patients with symptoms attributable to dissection and for operative planning. As previously discussed, routine follow-up for acute dissection occurs on a scheduled basis and is usually done with either CT or MRI. We prefer CT scanning for patients with normal renal function and no contrast allergy because CT is usually the original imaging study obtained during the acute dissection. The improved accuracy that comes with comparing similar studies combined with the availability, cost, and patient satisfaction make CT favorable for this purpose. MRI is utilized mostly as a follow-up study for patients with renal insufficiency but is the study of choice to provide precise anatomical detail for operative planning. Transthoracic echocardiography is useful to follow chronic type A dissection when there is aortic insufficiency. It can provide cross-sectional images of the ascending aorta but generating images useful for comparison to previous studies is highly dependent on the skill of the operator. For that reason, we use echocardiography to follow patients with aortic insufficiency but also obtain a CT scan to assess ascending aortic diameter. Aortography is used primarily for operative planning. Patients older than 50 years and those with risk factors for coronary artery disease routinely undergo coronary arteriography prior to operation and images of the aorta are obtained at that time. Aortography is especially useful to determine the origin of aortic branch vessels for operative planning when noninvasive imaging is inadequate (Fig. 45-21).



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FIGURE 45-21 Coronal view of contrast enhanced MRI (A) demonstrating chronic type B dissection with renal arteries (arrowheads) separated by dissection flap (arrow). Aortogram (B) of the same patient revealing that each renal artery is perfused exclusively by either the true or false lumen. Such tests are often complementary and may influence surgical strategy.

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Natural History

Chronic type A dissection develops in patients who fail to undergo immediate surgical treatment of the acute dissection. In contrast, chronic type B dissection may occur in patients successfully treated medically for the acute process and in those with repaired type A dissection who have a retained dissected descending thoracic aorta. The natural history of acute dissection rarely involves spontaneous healing. This phenomenon is observed in 4% to 31% of medically treated patients. Many patients with distal communication of the false lumen go on to develop aneurysmal dilatation of the aorta. The natural history of this process has been examined and reveals that there is an annual rate of expansion of 2 to 3 mm per year in communicating dissections and the rate is 1 mm per year in those not communicating. Despite appropriate medical management and close follow-up, 20% to 40% of patients with chronic dissection require operation for aneurysmal dilatation at 10 years. This number is probably even higher in those patients with connective tissue disorder. In one study of 50 patients over a period of 40 months, 18% had fatal rupture and another 20% underwent surgical repair because of symptoms or aneurysm enlargement, emphasizing the need for diligent follow-up care. Risk factors for rupture of chronic type B dissection in that study included older age, COPD, hypertension, and marginally pain. Chronic beta-blocker treatment reduces the rate of aortic dilatation as well as the incidence of dissection-related hospital admissions and procedures.39

Operative Indications

The operative indications for chronic type A and B dissection are shown in Table 45-4. Chronic type A dissection is rarely symptomatic yet a minority will present with chest pain as a result of aneurysm expansion or heart failure related to aortic regurgitation. Chronic type B dissection may also present with back pain or infrequently with a malperfusion syndrome. While each of these findings is an indication for intervention, the most common indication for surgical management is aneurysmal dilatation. The Yale group recently reviewed the size criteria indicating operative intervention for thoracic aortic aneurysms.40 These criteria dictate replacement should be performed for ascending aortic size greater than 5.5 cm, or 5 cm if a connective tissue disorder is present. Similarly, the two most frequent indications for operative repair of chronic type B dissection are aneurysmal dilatation and malperfusion. In the descending thoracic aorta, replacement is indicated at 6.5 cm, or 6 cm if there is a family history or physical stigmata of a connective tissue disorder. Eccentricity of the aorta was also predictive of rupture as was rapid expansion (more than 1 cm per year) and continued smoking. Such factors should therefore be considered when deciding to operate based on aneurysm size alone.

Operative Technique

GENERAL CONSIDERATIONS

The purpose of operation in chronic aortic dissection is to replace all segments of dissected aorta at risk for rupture and to prevent the possibility of subsequent malperfusion syndrome. The conduct of the operation including surgical approach, monitoring lines required, anesthetic technique, and cardiopulmonary bypass is similar to that described for acute dissection. Aprotinin or epsilon aminocaproic acid is routinely administered even in cases using deep hypothermic circulatory arrest. Greater emphasis is placed on methods of cerebral and spinal cord protection and various technical differences exist for aortic valve preservation and to avoid postoperative malperfusion.

CEREBRAL AND SPINAL CORD PROTECTION

The incidence of paraplegia following repair of thoracoabdominal aneurysms resulting from aortic dissection is reportedly as high as 10%. Both mechanical and pharmacologic interventions have been advocated over the last decade to reduce this risk. It appears that partial left heart bypass alone as previously described is sufficient for patients with aneurysmal dilatation of the thoracic aorta above the level of T9 and results in a paraplegia rate between 5% and 8%.41 Aneurysms involving the distal aortic arch require full cardiopulmonary bypass and deep hypothermic circulatory arrest for spinal cord protection. In such cases and in the case of the more extensive thoracoabdominal aneurysms, additional measures have variably reduced paraplegia rates lower than observed with cord hypothermia alone. Drainage of cerebrospinal fluid as described by Safi et al is routinely used in our practice for aneurysms extending lower than T9. Reimplanting intercostal and lumbar arteries between T9 and L1 is also important.42 The aortic cross-clamp is moved progressively distal to perfuse branches as they are implanted. Preoperative identification of the anterior spinal artery origin has been suggested but the combination of distal perfusion, cerebrospinal fluid drainage, and reimplanting large intercostal and lumbar arteries has provided adequate success at our institution. Additional techniques used for spinal cord protection include measurement of sensory and motor evoked potentials, regional epidural cooling, and the use of a variety of pharmacologic agents for cellular protection.

TECHNIQUES FOR TYPE A DISSECTION

Chronic type A dissection, with or without aneurysmal enlargement, is treated using similar operative techniques described for acute dissection. The particular operation performed depends upon the specific pathology involving the aortic root, status of the aortic valve, distal extent of dissection, and brachiocephalic vessel involvement. The pathology of each of these components can be very different in a chronic dissection as compared to the acute process. These differences underlie the need for surgical techniques appropriate to each unique abnormality. In general, the ascending aorta is replaced using a vascular graft to include the entire diseased segment as in acute dissection, but surgical treatment of the aortic valve and creation of the distal anastomosis differ.

Whereas the aortic valve can be repaired in most cases of acute type A dissection by simple commissural resuspension, the rate of aortic valve replacement is much higher in patients with chronic dissection. Preservation of the aortic valve is complicated by morphologic changes in the valvular apparatus such as leaflet elongation and annuloaortic ectasia, which render the valve irreparable in as many as 50%. More severe grades of preoperative aortic regurgitation portend a lower probability of valve preservation. In cases where the aortic valve cannot be preserved with simple commissural reattachment, three options exist to treat aortic insufficiency: composite valve-graft replacement, aortic valve replacement with separate ascending aortic replacement, and finally valve-sparing aortic root repair. The technical aspects of composite valve-graft repair were covered under acute type A dissection. Separate aortic valve and ascending aortic replacement are appropriate when there is an operative indication to repair the ascending aorta in the setting of a normal aortic root and structural aortic valve disease. Note that this operation is not appropriate for patients with connective tissue disease. In this situation aortic root replacement is required.

There are several methods for aortic valve preservation when aortic root replacement is indicated. One such technique is performed by reimplanting the valve commissures into an appropriately sized vascular graft, which is secured to the left ventricular outflow tract using multiple horizontal mattress sutures.43 A more elegant yet time-consuming technique requires resection of the sinuses of Valsalva leaving a 5-mm rim of aorta circumferentially around the leaflets. Scallops are then created in the vascular graft to resuspend the commissures and remodel the aortic root. David et al advocate Teflon felt reinforcement of the aortic annulus to prevent late annular dilatation and recurrent aortic insufficiency for the remodeling technique. The mid-term outcome of such operations revealed a freedom from reoperation of 97% to 99% at 5 years and a 5-year survival for the aortic dissection subgroup of 84%.44 Cochran et al devised a similar technique to recreate the sinuses of Valsalva which may be more important than previously recognized and contribute to improved long-term valve durability.45 Such data in patients with chronic dissection are lacking. These techniques appear appropriate for patients with Marfan disease and in those with congenitally bicuspid aortic valves.

Treatment of the distal aorta in chronic type A dissection is somewhat controversial. Some advocate obliteration of flow in the false lumen with distal aortic repair, whereas others purposely maintain flow into both the true and false lumen using distal resection of the intimal flap. Those who reunite the chronically dissected aortic layers to perfuse only the true lumen maintain that false lumen perfusion continues through distal reentry tears in over 50%. There is a theoretical concern that important side branches arise exclusively from the false lumen and perfusion may be interrupted with this technique. Our practice at the University of Virginia is to resect the distal chronic dissection flap to obviate such concerns. The distal anastomosis is therefore made to the outer wall of the aorta, which has a great deal of structural integrity. Malperfusion of the brachiocephalic vessels as a result of chronic type A dissection is treated with resection of the dissection flap from the arch. Infrequently, the chronic dissection flap extends into more distal branch vessels and may present as transient ischemic attacks or stroke. In such cases it is often necessary to resect the dissection flap into the branch vessel or reunite the layers distally prior to reimplantation.

Infrequently, chronic type A dissection results in extensive aneurysmal dilatation of the aorta extending from the ascending aorta through the arch and into the descending thoracic aorta. Surgical treatment of such extensive disease has traditionally been performed as a staged procedure in which the ascending aorta and arch are replaced first through a sternotomy. The second stage of the so-called elephant trunk procedure is performed 6 weeks later through a left thoracotomy for replacement of the descending aorta using a second vascular graft. Originally described by Borst et al, this technique has been used extensively with good results.46 In some cases, the aorta distal to the left subclavian artery may be so large as to preclude the use of a two-stage repair. Kouchoukos et al recently described a single-stage repair performed through a bilateral anterior thoracotomy in which the arch is repaired first during a brief period of circulatory arrest. Right subclavian and femoral artery cannulation for cardiopulmonary bypass provide proximal and distal perfusion during the subsequent ascending and descending aortic replacement. The hospital mortality was 6.2% and there were no adverse neurologic outcomes in this small series.47

TECHNIQUES FOR TYPE B DISSECTION

The techniques used for replacement of the descending thoracic aorta are identical to those described for treatment of acute type B dissection. The extent of resection, however, for chronic type B dissection is usually greater with the goal to remove all dissected aorta at risk for rupture or symptoms. Usually these operations can be performed through the left chest, but more extensive aneurysms or cases of visceral malperfusion require a thoracoabdominal incision or a staged repair similar to the elephant trunk. The proximal anastomosis is ideally made to undissected normal aorta but infrequently the distal arch is involved, which requires alteration in surgical strategy. Most of the technical controversy regarding repair of chronic type B dissection centers on methods of spinal cord protection during these operations.

As mentioned, we prefer the combination of partial left heart bypass and cerebrospinal fluid drainage. Sites for cannulation are the left inferior pulmonary vein and the left femoral artery or descending thoracic aorta. Depending upon location and extent of aneurysm, the distal arch is mobilized first. The area between the left common carotid and left subclavian artery is circumferentially dissected, and the left subclavian artery is independently controlled. Partial left heart bypass is then initiated. Ideally clamps are placed between the left subclavian and left common carotid arteries and on the aorta distal to the involved segment. If the entire descending thoracic aorta is diseased, the clamp is placed on the mid-thoracic aorta to perform the proximal anastomosis first. The aorta is opened and small intercostal arteries are oversewn. The proximal anastomosis is made to normal aorta whenever possible with running 3-0 Prolene; 4-0 Prolene is used if the tissue is fragile. The clamp is moved distally onto the graft to inspect the proximal anastomosis and achieve hemostasis. Several centimeters of the dissection flap is then resected from the lumen of the distal aorta and the distal anastomosis created to the adventitia of the chronic dissection. In more extensive thoracoabdominal disease, the clamp is progressively moved distal as intercostals arteries below T7 to L2 and visceral vessels are reimplanted (Fig. 45-22). Bypass is terminated and the operation completed.



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FIGURE 45-22 Replacement of the thoracoabdominal aorta. (A) A left femoral cannula perfuses the lower body and viscera while the heart continues to eject. The arch is transected near or at the left subclavian and any dissection involving the proximal cuff is repaired. The graft is sewn end-to-end to the proximal aorta. (B) The clamp is moved down and a second arterial cannula is inserted into the proximal graft to perfuse the upper body and heart. The anterior wall of the dissection is incised longitudinally and bleeding intercostals of the upper six pairs are oversewn. A group of lower intercostal arteries above the celiac axis is sutured to the graft. (C) The clamp is moved down and the distal aortic clamp is moved to the left common iliac artery. A patch of aorta containing the celiac, superior mesenteric, and right renal artery is sewn to an opening in the graft. The left renal artery is sutured separately to the graft. (D) The proximal clamp is moved below the visceral anastomoses and the distal aortic anastomosis is made to the aortic bifurcation. (Reproduced with permission from Stone C, Borst H: Dissecting aortic aneurysm, in Edmunds LJ Jr (ed): Cardiac Surgery in the Adult. New York, McGraw-Hill, 1997; p 1125.)

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Full cardiopulmonary bypass with deep hypothermic circulatory arrest may be necessary in cases where the proximal anastomosis cannot be safely or adequately performed with a clamp in the usual position. Kouchoukas et al have a large experience in this area and cite a 6.2% 30-day mortality, 1.9% stroke rate, and no paraplegia in the subgroup of patients with aortic dissection.48 These data strongly support this simple and elegant technique as one of the most efficacious for spinal cord and visceral organ protection in these complicated procedures.

Results

The operative mortality for chronic type A dissection is between 4% and 17% and on average is very similar to that reported for chronic type B repair at 11% to 15%.37,49 The actuarial survival following operation for chronic type A and B dissections is not different at 5 years (59%75%) or at 10 years (45%).38 The stroke rate following repair of chronic type A is 4%. Early neurologic complications occurred in 9%.49 Regular follow-up of the aortic valve is necessary when the native valve is preserved at the initial operation. This is best performed using transthoracic echocardiography on a yearly basis. Early reports indicated that nearly 20% of patients require reoperation secondary to progressive aortic regurgitation. The most recent data from David et al, however, reveal a 90% ? 4% 5-year freedom from severe or moderate aortic insufficiency in patients with aortic root aneurysm and 98% ? 2% in patients with ascending aortic aneurysm following valve-sparing operation.50


?? CONCLUSION
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Considerable improvement in the treatment of patients with acute and chronic aortic dissection has occurred over the last 50 years. Continued progress is inevitable and technologies such as endovascular repair may eventually achieve results comparable to surgery. Complex forms of dissection that include aortic root and valvular pathology, however, will require surgical treatment for the foreseeable future. These patients will undoubtedly benefit from the novel basic and clinical research taking place in the areas of spinal cord and cerebral protection, strategies for cardiopulmonary bypass, improved vascular graft technology, and procedures for preservation of the aortic valve. Such progress may even permit advancement in our greatest remaining clinical challenge, those patients who are hemodynamically unstable following aortic dissection.


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