Chapter 30. Aortic Dissection

• Acute aortic dissection occurs more commonly than ruptured abdominal aortic aneurysm.
• The typical pain, poor peripheral perfusion, and evidence of aortic branch occlusion suggest the diagnosis.
• Early pharmacologic control of systolic blood pressure and the pulse wave (dP/dT) is imperative.
• Investigations must be undertaken urgently to confirm the diagnosis and direct definitive treatment.
• Emergency surgical repair is indicated for type A dissections.
• Control of hypertension is important to minimize complications and maximize survival both in the postoperative period and in the long term.
• Type B dissections may have a more ominous prognosis than previously thought and require very close long-term follow-up.

Aortic dissection is the most common catastrophe affecting the aorta, occurring two to three times more commonly than acute abdominal aortic aneurysm rupture.1 The reported incidence is approximately 10 to 20 per 1 million per year.2 Rarely is the outcome of a cardiovascular disease so dependent on the skills and cooperation of the emergency room physician, the cardiac surgeon, and the intensivist as it is with acute dissections of the aorta. Maximal survival depends on a high index of suspicion of the diagnosis despite a myriad of different presentations, early pharmacologic intervention for control of hypertension, rapid diagnosis with definitive imaging, and then appropriate relegation to medical or surgical management depending on the dissection type. Without treatment, the 3-month mortality is 85% to 90%, but with the appropriate treatment, survival rates of over 80% can be expected.

Previously, aortic dissections were referred to as dissecting aneurysms, as originally coined by Laënnec. This is a misnomer in that the pathology is a dissecting hematoma that separates the intima and inner layers of the media from the outer medial and adventitial layers (Fig. 30-1). The intima is therefore not aneurysmal, and is if anything, narrowed. Blood invades the media through a tear in the intima and proceeds ante- or retrogradely through the aortic wall, forming a false lumen. The hematoma spirals around the right and posterior aspects of the ascending aorta, supraposteriorly along the arch, and then down the left and posterior aspects of the descending aorta.3 The hematoma may then have several serious sequelae. It may rupture into the pericardial space causing tamponade, or into the pleural space with exsanguinating hemorrhage. This occurs less frequently than expected because the adventitial layer represents 66% of the overall strength of the aortic wall. It may also cause occlusion of aortic branch arteries or prolapse of one or more of the aortic valve cusps, resulting in acute aortic insufficiency.

Generally the tear is due to either a weakening of the wall of the aorta, an increase in luminal shear stress, or both.3 Weakening of the aortic wall occurs as the result of medial degeneration or iatrogenic injury. Medial degeneration (cystic medial degeneration or necrosis) is manifested by the loss of smooth muscle cells and accumulation of basophilic amorphous material with or without associated “cysts” in the aortic media. This is believed to be due to inborn errors of metabolism (Marfan's or Ehlers-Danlos syndrome). There is a reduction in the cohesiveness of the layers of the aortic wall as a result. Other causes of reduced wall strength causing aortic dissection include annuloaortic ectasia, bicuspid aortic valve, coarctation, and pregnancy (especially in the third trimester.)

Iatrogenic injuries occur during open heart surgical procedures at any point where the aorta is invaded, such as the aortotomy for an aortic valve replacement or the proximal anastomosis of an aortocoronary bypass graft.

Stresses applied to the aortic wall increase wall tension and lead to dissections. Most important are intraluminal shear stresses, which are related both to the level of the systolic blood pressure and to the steepness of the aortic pulse wave.2 This is referred to as dP/dTmax and represents the speed with which the maximal systolic pressure is attained in the aortic root. As this increases, so too does the shear stress on the ascending aorta.

Dissections are classified by timing and location to identify the morbidity and mortality for the specific lesions.

Timing

• Acute: <2 weeks
• Chronic: >2 weeks

Acute dissections are very high-risk lesions, with an estimated mortality of 50% for the first 48 hours (or 1% per hour).

Location

• Type A: The ascending aorta is involved independent of the site of the intimal tear (since 15% of transverse arch and 5% of descending aortic tears will involve the ascending aorta), and may include the aortic arch and part of or all of the descending thoracic and abdominal aorta.
• Type B: Descending aorta (beyond the left subclavian artery).

This classification system, proposed by Daily and colleagues and popularized by the Stanford group, replaces the original system proposed by DeBakey (Fig. 30-2). Using this classification, 60% of all dissections are type A, and 40% are type B. The classification system is based on the risk of sudden death from the dissection, which is highest in type A. Here the dissection may cause tamponade or severe aortic insufficiency with congestive heart failure, as well as coronary thrombosis, especially involving the right coronary artery with acute myocardial infarction. Type B dissections do not have these risks and generally can be approached and managed conservatively. As a result, therapeutic interventions are dependent on location, with almost all type A dissections requiring urgent operative intervention, whereas type B dissections are managed primarily pharmacologically, with surgery only for specific complications. However, recent evidence suggests that up to 40% of type B dissections can lead to late death, and there is great interest in endovascular stenting to improve long-term survival.4–6

Aortic intramural hematoma (IMH) results from hemorrhage within the aortic wall without disruption of the intima. It is likely due to rupture of the vasa vasorum and may progress to rupture through the intima to form a classic dissection in up to 33% of cases.7 It is an entity that is frequently confused with aortic dissection whose diagnosis, management, and prognosis remain debatable. Most authors believe the clinical course is similar enough to warrant treatment of IMH the same as a classical dissection.8–10 A high percentage (up to 80%) may completely resolve within 1 year, but up to 60% of the remaining patients can go on to develop saccular aneurysms within 45 days with a significant annular growth rate.8,10 The diameter of the aorta is important in that if the aortic diameter is <45 mm at 1 month follow-up, then most will resolve. Complications appear to occur mainly in patients with an aortic diameter over 45 mm.9

Men, particularly black men, are at two to three times the risk of developing an aortic dissection as women. More than 90% will have a history of hypertension requiring treatment. The presentation of an acute dissection can be subtle, demanding great attention to detail to make the diagnosis, or classic and obvious. A new murmur of aortic insufficiency is present in 50% to 66% of type A dissections11 due to the loss of support of the valve at the commissures as the inner layer of the aorta collapses inward. A continuous murmur suggests rupture of the dissection into the right ventricle or atrium.12 The signs and symptoms are related to the location of the tear and the extent of the hematoma dissection. These are manifested mainly by pain, poor peripheral perfusion despite an increased blood pressure, and signs and symptoms of aortic branch occlusion.

Pain

Typically, the pain is either retrosternal, or central interscapular back pain, but it may be epigastric. Classically, it begins in the chest, moves to the back, and then moves down to the abdomen or lower extremities as the dissection progresses, but this pattern is rarely seen. Patients describe the pain as “sharp,” “tearing,” or “knife-like,” and it is most often excruciating in intensity. To differentiate it from angina, the pain is maximal immediately upon onset, and it is difficult to obtain complete relief with opiates alone. Clinical diagnostic accuracy may approach 90% if three basic questions are asked regarding the pain's quality (tearing or ripping), radiation (beginning between the scapulae and radiating down the back), and the intensity at onset (abrupt onset of 10/10 pain).3

Poor Perfusion

Patients frequently present with evidence of shock, with a cool, clammy periphery, ashen coloring, and depressed level of consciousness, and yet markedly elevated systolic blood pressure frequently exceeding 200 mm Hg. Most often this is due to reflex sympathetic discharge from the intense pain. It can occur, however, with myocardial infarction due to coronary artery occlusion by the dissection, or from severe aortic insufficiency with congestive heart failure, which is present in 30% to 60% of patients with type A dissections. If the blood pressure is depressed, the dissection may have ruptured into the pericardium with tamponade (as occurs in 30% of type A dissections) or into the pleural space (left more often than right) in type B dissections, with resulting hypovolemia.

Signs and Symptoms of Aortic Branch Occlusion

Approximately one third of all patients will present with compromised flow to a major branch of the aorta as part of their presentation.14 The vessel may be sheared off or compressed, resulting in occlusion and/or thrombosis, or be perfused through the false channel (Fig. 30-3). Table 30-1 lists the vessels affected and the manifestations. The dissection usually travels in a spiral motion down the thoracic aorta such that the celiac axis, superior mesenteric artery, and right renal artery remain intact. In type A dissections the innominate artery (and thus blood flow to the right carotid artery to the brain, causing cerebrovascular insufficiency, and the right subclavian artery to the right upper extremity, causing a pulse deficit) are the most frequently affected. A measured brachial pressure differential of greater than 20 mm Hg is an independent predictor of the presence of a dissection.5 The dissection usually stops at the level of the iliac arteries, with the left iliac more often affected, leading to compromised blood flow to the left leg. Rarely is there only one tear in the aorta, and more commonly, the dissection has multiple re-entry sites along its path down the aorta. The common femoral arteries are seldom dissected, an important issue at surgery, since cannulation of the femoral artery is necessary for placing the patient on cardiopulmonary bypass.16 Fortunately, the visceral and renal vessels are affected in less than 3% of patients, since their involvement denotes a much increased mortality rate of 41% versus 27%.17

Neurologic sequelae are of particular concern. Some neurologic dysfunction, such as depressed level of consciousness or dizziness, is said to occur in 30% to 50% of patients.3 However, concrete focal neurologic deficits occur much less frequently (<10% overall), and may affect the central nervous system (CNS), spinal cord, or peripheral nerves. CNS deficits range from minor transient ischemic attacks to deep coma. Cerebrovascular accidents (CVAs) causing hemiparesis affect 5.5% to 6.7% of patients with type A dissections. They are primarily due to innominate–carotid artery occlusion, with the right side affected in two thirds of cases. They also can be caused by emboli or low flow with thrombosis due to previous carotid stenosis. Paraparesis and paraplegia fortunately are rare (2% of type A), because they portend a very poor prognosis.

Occasionally patients may present with vascular compromise foremost in their complaints and findings. A patient suffering an acute occlusion of blood flow into their lower extremity, particularly the left, with no definite clot or embolus found at surgery should be strongly suspected of having a dissection and investigated immediately. Unfortunately the physical findings classically associated with dissection are present in less than half of all cases, thereby necessitating a high index of suspicion to save these patients.18

Laboratory

Laboratory data are usually within normal limits in patients with acute dissection. The white blood cell count may be slightly elevated to 12,000 to 20,000/μL, most likely as a stress response. Electrocardiogram (ECG) interpretation may show left ventricular hypertrophy due to chronic hypertension, but other changes are rare. Acute ischemic changes should raise the concern of coronary artery involvement by the dissection in the patient with a typical history. Conversely, to avoid the dire consequences of misdiagnosis, any patient presenting to the ER with ECG changes suggesting myocardial ischemia (especially with evidence of right coronary artery involvement) should have their history considered carefully before immediately moving to anticoagulation, thrombolytics, and urgent cardiac catheterization to treat the more prevalent condition of atherosclerotic coronary artery disease.

Diagnostic Imaging

Diagnostic imaging is the most important investigation for the diagnosis and classification of aortic dissections. Standard anteroposterior and upright lateral chest x-rays often reveal a widened mediastinum, although this may be absent in up to 40% of type A dissections (Fig. 30-4). Classically, the aorta bulges to the right with type A and to the left with type B dissections. Occasionally a double rim of calcification may be present in the distal aortic arch or a pleural effusion may be present (left more than right), due mainly to a serous sympathetic reaction rather than to frank blood from a rupture.

Significant debate exists as to the best imaging modality presently available for aortic dissections. The ideal modality would be readily available, easy to interpret, represent no risk to the patient, and provide all the information the surgeon requires. These needs include assessment of the ascending aorta, identifying the site of the intimal tear, the full extent of the dissection, existence of branch vessel involvement, presence of a pericardial effusion, and presence and severity of aortic valve insufficiency.19 Several imaging techniques including aortography, computed tomographic (CT) scanning, magnetic resonance imaging (MRI), and echocardiography are highly accurate for the diagnosis and classification of dissections.20 Controversy exists as to which of these is the most accurate.19,20–24 In the past many authors believed that aortic angiography was the most definitive diagnostic method, with sensitivity and specificity of 88% to 90% and 90% to 95%, respectively.2,25 In addition to confirming the diagnosis by illustrating the true and false channels, the aortogram could pinpoint the site of the intimal tear (Fig. 30-5), establish the extent of the dissection, quantitate the severity of aortic insufficiency if present, and identify the presence and degree of aortic branch occlusions. Some authors, however, have expressed concerns over false-negative reports due to viewing the flap and both lumens en face, with the central beam missing a small localized dissection, and possibly missing the flap due to simultaneous opacification of both true and false lumens.12 The procedure is also invasive and requires a contrast load, so less invasive investigations are preferred.

CT scanning is a noninvasive technique that yields excellent images of dissections, especially type B. Specific identification of true and false lumens with a flap is possible, as well as detection of pericardial effusions and accurate depiction of the extent of the dissection (Figs. 30-6 and 30-7). The new third-generation helical CT scanners yield excellent images both in two and three dimensions (Fig. 30-8). CT is very specific and accurate (∼100%) for the diagnosis of dissection,18,25 and 96% accurate for the presence of aortic branch involvement.19 CT scanning does not yield information regarding aortic insufficiency or left ventricular function, and requires both contrast administration and exposure to radiation. CT scanning is also inferior to aortography for identifying the site of the intimal tear. Recently, however, the site of the intimal tear has had debatable bearing on the type of dissection or surgical success. Since CT scanning lacks somewhat in sensitivity, if the CT scan is negative and the suspicion of aortic dissection remains high, other investigations should be done to rule out a dissection. Helical CT scanning is the author's recommended imaging technique for the long-term follow-up of the patient, given its low expense, high reproducibility, and minimal patient discomfort.

Echocardiography is likely the diagnostic modality of choice for acute aortic dissections. Both transthoracic and transesophageal two-dimensional echocardiography can accurately evaluate the most important issues of dissections; involvement of the ascending aorta, presence and severity of aortic insufficiency, the entry sites in the intimal flap, and presence of aortic arch dilation. Two lumens may be seen separated by a flap, or there may be central displacement of intimal calcification. The addition of color-coded Doppler allows better identification of the true and false lumens, even if the false lumen is thrombosed. The presence of a pericardial effusion and any left ventricular wall motion abnormalities also may be assessed accurately. Transesophageal echocardiography (TEE) was previously criticized for being unable to visualize the aortic arch, but current multiplanar TEE transducers have few blind areas. Its main limitation is inability to see the intra-abdominal aorta, but this can be assessed with simple ultrasound.23

Transthoracic echocardiography is less accurate than transesophageal echocardiography in the diagnosis of aortic dissections. It is also frequently technically limited due to chest wall abnormalities, chronic obstructive pulmonary disease, and obesity.

TEE21,23 is the most efficient and accurate diagnostic modality available (Fig. 30-9). Its sensitivity and specificity are over 98%, so this technique very accurately identifies the presence or absence of a dissection. Notably, it can be performed in less than 30 minutes in an emergency room or intensive care unit. The efficiency and mobility are very important in the management of critically ill patients, who are best cared for in a well-monitored ICU rather than in the radiology suite. Occasional complications (<1%) have included transient arrhythmias (atrioventricular block, bradyarrhythmias, or premature ventricular contractions), reports of rupture of the dissection during the insertion of the probe, and esophageal perforation. Generally the procedure is well tolerated with appropriate control of pain and hypertension.21,22,24

MRI is very accurate, sensitive, and specific in dissections, but has been used sparingly as the procedure requires 45 minutes and can be difficult due to limited access to a critically ill patient.19,23–25 It is, however, the only modality that provides all of the previously mentioned preoperative needs of the surgeon. It is noninvasive and does not require contrast material or ionizing radiation. Excellent contrast can be obtained between extraluminal structures, and it allows the visualization of vascular walls and both clotted and flowing blood. MR technology is advancing rapidly, with accuracy of 100% with phase-contrast cine MR angiography,1–9 and new MRI sequences (such as the breath-hold gradient-echo) have been able to reduce the procedure time to less than 5 minutes without compromising accuracy.26

The author presently recommends TEE as the initial investigation. If this is not immediately available, then a helical CT scan of the thorax is performed. If this is negative and there is still a strong suspicion of dissection, then MR angiography may be performed in a stable patient. Of course, this approach should be modified by availability and the local expertise with these imaging techniques at each institution.

Untreated acute type A aortic dissections have a uniformly poor prognosis. Fifty percent of patients die within the first 48 hours, and <10% will survive 1 month. Poor prognostic variables include aortic branch complications (particularly mesenteric and renal arteries), type A dissections, associated coronary artery disease (CAD), and neurologic deficits (CVA and paraplegia).27

Hemodynamic instability (systolic BP <90 mm Hg) represents a 32% mortality vs. 8.5% for those with stable hemodynamics.8

To maximize survival, optimal treatment of acute dissections must include early pharmacologic control of blood pressure and pain, often before the definitive diagnosis is made, combined with appropriate surgical intervention. All patients with aortic dissections must have intensive monitoring in a critical care setting. The patient should be placed on a cardiac monitor, and have an intra-arterial catheter (for ongoing blood pressure control), and central venous pressure and urinary catheters inserted. Blood should be drawn for standard laboratory investigations as well as cross and typing for blood transfusion in case surgery is needed. The patient should be observed closely for any change in hemodynamic parameters or neurologic function and for evidence of organ ischemia.

Intravenous antihypertensive agents are used to reduce the level of systolic blood pressure and the pulse wave (dP/dTmax) to halt the progression of the dissecting hematoma. With the hematoma stabilized, pain usually can be controlled with intravenous opiates. Several agents are available for the ICU control of systolic blood pressure and dP/dTmax, and these are listed in Table 30-2 along with their suggested mechanism of action and duration of activity.

Labetalol remains the first choice in antihypertensive agents for aortic dissections. It is a selective α1 nonselective β1- and β2-adrenoreceptor blocker, and so reduces dP/dTmax and systolic blood pressure by β-blockade and vasodilation. It can be delivered by bolus (as preferred by most authors) or continuous infusion, even in the ER setting. Its peak reduction in systolic blood pressure occurs within 5 minutes, and its duration of action is 2 to 12 hours. It is suitable for long-term control of hypertension in oral form.

Esmolol, an ultra-short-acting β-blocker with β1-selective adrenergic receptor blockade, is extremely useful for the acute control of hypertension in patients with dissections. Its very rapid onset (decrease in heart rate in less than 2 minutes) and short duration of action (half-life of 9 to 10 minutes) allow for tight control of blood pressure, especially in labile patents.

If labetalol and esmolol are not available, then sodium nitroprusside and propranolol hydrochloride may be used. Propranolol must be given because nitroprusside increases dP/dTmax through a sympathetic reflex from its peripheral vasodilatory effects when used alone.

Patients who cannot tolerate β-blockade (e.g., those with severe asthma, decompensated congestive heart failure, or bradycardia) may be treated with trimethaphan camsylate. In order to adequately reduce the systolic blood pressure, it may be necessary to elevate the head of the bed or dangle the patient's legs over the side of the bed. Occasionally, trimethaphan may need to be combined with reserpine or guanethidine. It has many sympathoplegic side effects and can drop the blood pressure quite precipitously. Tachyphylaxis occurs quickly.

Systolic blood pressure should be reduced to levels that will halt the progression of the dissection. Most authors agree that a systolic blood pressure of 90 to 100 mm Hg is desirable as long as the patient has adequate organ perfusion, as evidenced by a clear sensorium, good urine output, and the absence of lactic acidosis. If respiratory distress occurs that requires high doses of opiates and benzodiazepines, the patient should be intubated by an experienced cardiac anesthesiologist to minimize changes in heart rate and blood pressure.

Acute aortic dissections, especially type A, are extremely dangerous lesions that may become complicated with rupture and death at any moment. Investigations should be performed expeditiously to determine the dissection type and the presence of aortic branch complications. Patients with type A dissections should be offered urgent surgical intervention for maximal survival. Relative contraindications to surgery include severe organ dysfunction such as diffuse coronary artery disease, end-stage chronic obstructive pulmonary disease, old age (for those over age 80 the risk rises markedly, perhaps as high as 80%),29 moribund patient, paraplegia, and CVA. Whether an acute CVA represents a contraindication to surgery is controversial. CVA does represent an independent negative influence on survival. Surgery may make the neurologic deficit worse due to intraoperative bleeding from heparinization, embolization, or reperfusion injury when the occluded carotid is reopened. Without surgery, however, these patients have a near uniformly fatal prognosis. It has been shown that the presence of the CVA does not increase the risk of mortality with surgery. Shumway's group30 found 85% of survivors to be improved or unchanged neurologically, and suggested that there is no way to predict neurologic outcome from the preoperative neurologic status. A CVA is therefore only a relative contraindication to surgery, and only deeply comatose or moribund patients should be refused definitive surgical repair.

Aortic branch complications in type A dissections are best managed by surgically restoring flow to the true lumen by definitive repair of the dissection and postoperative assessment for persistent ischemia.14 Less than 10% of patients will require further procedures for persistent ischemia after definitive repair of the dissection. Rarely, organ hypoperfusion may continue, necessitating emergent fenestration (creating communication between the true and false lumina) of the abdominal aorta, ideally by an interventional radiologist with cutting balloons.4

Type B dissections are generally best managed by intensive medical treatment of blood pressure, with surgery reserved for complications of the disease. These complications are a result of progression of the dissection despite maximal medical therapy. Intervention is recommended if the aorta increases in size or if evidence of organ ischemia due to aortic branch occlusion (e.g., abdominal pain, renal dysfunction, or lower extremity ischemia) exists. Intractable pain, evidence of a new pleural or pericardial effusion, acute saccular aneurysms, or a rapid increase in size over a period of hours indicates impending or frank rupture, and emergent surgical repair (or endovascular stenting if available) is imperative for survival.

This conservative approach has been challenged.27 The surgical mortality in acute type B dissections was reported to be reduced from 38% to 13% in a small group of patients. This would be an improvement over medical therapy alone, which incurs a 20% mortality. A larger experience is necessary before this aggressive approach is adopted for all type B dissections. Similarly, stent-grafts have been inserted in the acute setting with good early but unsatisfactory long-term results.4–6

Dr. Michael DeBakey is credited with the initial surgical successes in the treatment of acute aortic dissections. The procedures can be considered as being separate for type A and type B dissections.

Type A

The surgical procedures for type A dissections are designed to treat the life-threatening complications in the ascending aorta. There are many factors that are important for deciding the appropriate surgical procedure for each patient. Many of these can be identified preoperatively, such as the presence of a preexisting abnormality and/or competency of the aortic valve, patency of the coronary arteries, size of the aortic arch, quality of the aortic tissue (e.g., Marfan's or Ehlers-Danlos syndrome), and presence or absence of associated aortic branch compromise (Figs. 30-10 and 30-11). The surgical options include simple graft interposition, resuspension of the aortic valve and graft interposition, replacement of the aortic valve and supra-sinus graft interposition, and valved-conduit graft insertion (Bentall procedure).

General preparation of the patient for the procedure includes continuous monitoring of arterial and central venous pressures and usually insertion of a pulmonary artery catheter and a transesophageal echocardiography probe. The patient is placed on cardiopulmonary bypass (CPB) by inserting the arterial cannula into either a femoral artery (usually the right) or the right axillary artery31 to leave the ascending aorta and aortic arch clear for surgical repair. Through a median sternotomy, the patient undergoes continuous CPB and may require hypothermic cardiac arrest or deep hypothermia (15° to 18°C) and total circulatory arrest.32

Many surgeons feel it is important to resect the area of the tear in the aorta and thus use total circulatory arrest for all cases, especially for the distal anastomosis when replacing part or all of the aortic arch.3–1 The time spent with the circulation arrested ideally should be kept to less than 45 minutes to minimize organ dysfunction. The brain is the most sensitive of the body's organs to prolonged circulatory arrest, so several methods have been proposed to improve cerebral protection. Selective antegrade perfusion of the innominate and left carotid arteries, as well as retrograde perfusion by cannulating the superior vena cava are utilized for periods of more prolonged arrest.33–36

Suprasinus graft interposition is performed for dissections not involving the aortic valve and without gross dilatation of the aortic arch. It involves interposing a woven Dacron tube graft from just above the aortic valve (at the level of the sinotubular junction) to the innominate artery (Fig. 30-12). The aortic wall may be reinforced with fibrin glue and/or felt to increase the strength of these friable tissues.

Resuspension of the aortic valve with suprasinus tube graft replacement of the ascending aorta is indicated for aortic insufficiency in patients without connective tissue abnormalities. The aortic valve commissures are tacked back to the outer wall of the aorta (Fig. 30-13) so as to return the cusps to their normal position and restore competency to the valve. The patient's own aortic valve is preserved and is most often competent.37 The ascending aorta is then replaced with a tube of Dacron. If the aortic arch is not frankly aneurysmal, the graft is sutured to the distal ascending aorta.

Valved-conduit grafts consist of a prosthetic valve attached to a Dacron tube graft (Fig. 30-14). This procedure was popularized by Bentall and requires replacement of the aortic valve and ascending aorta and insertion of the left and right coronary arteries into the graft. The Bentall procedure is indicated for underlying disease of the aortic wall where there is a high risk of later aneurysmal dilation of the aorta, as in Marfan's or Turner's syndrome and annuloaortic ectasia. It is also indicated for tears arising close to the coronary sinuses or if the native aortic valve is diseased. The prosthetic valve may be either mechanical or bioprosthetic. The most popular mechanical valves are bileaflet such as those made by St. Jude Medical. These are placed primarily in young patients (<60 years old) in whom there are no contraindications to anticoagulation, as they require lifelong warfarin therapy. Older patients or those with contraindications to anticoagulation may have a bioprosthetic-valved conduit inserted, such as the Carpentier-Edwards porcine valve.

Each of these procedures may involve extensive replacement of the aorta to include the aortic arch, in whole or in part. This adds to the risk of the operative procedure, but if the arch is grossly aneurysmal, freedom from late operation and overall survival are increased significantly with immediate repair.38

Rarely, in cases of extensive aneurysmal dissections involving the ascending aorta, arch, and descending portions of the thoracic aorta, an “elephant trunk” technique must be used.39 This requires replacement of the ascending aorta and the arch with a graft (Fig. 30-15), with the addition of several inches of telescoping redundant graft beyond the distal anastomosis and down the descending aorta. At a later date the patient has the rest of the descending thoracic aorta replaced through a left thoracotomy utilizing the free end of the redundant, previously placed graft. Dr. Lars Svensson of the Cleveland Clinic has a novel and successful approach to these difficult cases, using stent-grafts to manage the descending thoracic portion of the dissection when aneurysmal. After the patient has recovered from the elephant trunk procedure they return to have a stent-graft placed endovascularly from below and attached to the free end of the “trunk,” thereby avoiding the difficult and risky thoracic surgical procedure. Of great interest is that Dr. Svensson has utilized this procedure with excellent results for isolated type B dissections in patients who would not tolerate surgical repair.

The resolution of aortic branch complications should be assessed at the end of the procedure. Pulses should be checked over both carotids and the radial and femoral arteries. If concerns exist for the presence of ongoing ischemia, then immediate surgical revascularization should be undertaken. This usually involves an extra-anatomic reconstruction such as axilloaxillary bypass for upper limb ischemia or femorofemoral bypass for unilateral lower limb ischemia. Aortic fenestration is necessary for bilateral lower extremity or renal ischemia. This can be done either surgically, or perhaps preferably by catheter-based techniques in the radiology department. Surgically this involves opening the abdominal aorta and resecting a portion of the inner wall (consisting of intima and part of the media) so as to allow flow through both the true and false lumens to restore blood flow. With the catheter-based technique, catheters are placed up both lumens and a cutting balloon creates the fenestration between the two.4

Type B

Repair of dissections involving the descending thoracic aorta is undertaken for failure of medical therapy to control the progress of the dissecting hematoma (i.e., rupture or aneurysm formation) and for aortic branch compromise. Replacement of the descending thoracic aorta is usually necessary from the left subclavian artery down to middle or lower thoracic levels (Fig. 30-16). The entire descending thoracic and abdominal aorta may require replacement if it is involved with the dissection and becomes diffusely aneurysmal. This requires the reimplantation of the arteries supplying the spinal cord, especially the artery of Adamkiewicz (usually arising between the ninth thoracic and second lumbar segments of the aorta), as well as the neighboring intercostal arteries. Even this does not ensure protection from spinal cord ischemia and resulting paralysis.40 All renal and visceral vessels must be reimplanted into the graft as well. The surgery is performed through a left thoracotomy or thoracoabdominal incision and requires single-lung anesthesia and cross-clamping of the aorta at the level of the left subclavian artery. The aorta is opened and replaced with a long Dacron tube. Controversy exists as to protection of the spinal cord during aortic cross-clamping. The concern is to maintain blood flow to the distal aorta and so to the collateral vessels to the cord. Although many options exist, the most popular are some form of CPB (using femorofemoral or atriofemoral bypass), intraluminal shunt (Gott), partial drainage of cerebrospinal fluid,41–43 and the simple clamp-and-sew technique. However, no technique has been shown to be superior to the others in reducing the high risk (∼40%) of paraplegia with surgical repair of acute type B dissections.

Stent-grafting of the descending thoracic aorta has been experimented with in both acute and chronic dissections. Between 20% and 40% of patients who survive the acute phase will go on to aneurysm formation within 2 to 5 years, significantly impacting their survival.44 Aortic stent-graft placement allows for occlusion of the intimal entry tear by implantation of a membrane-covered (Dacron), self-expanding (usually nitinol) stent (see Fig. 30-15C) to initiate progressive thrombus formation within the false lumen and resultant aortic remodeling.4 Unfortunately, despite good initial procedural success with few complications, long-term results and complications have thus far limited enthusiasm for this approach until marked improvements are made in both the delivery system and the stent-grafts themselves.

Consideration should also be given to the management recommended by Dr. Svensson and illustrated in Fig. 30-15, which combines an elephant trunk procedure with stent-grafting of the descending aorta.

Morbidity

Patients undergoing surgical repair of aortic dissections are subject to the same postoperative complications as with any open-heart procedure. Early complications include myocardial infarction, low-output syndrome (systolic BP <90 mm Hg with an elevated pulmonary wedge pressure requiring inotropic support), arrhythmia, bleeding, respiratory complications (prolonged ventilation, atelectasis, and effusion), stroke, and renal failure. Complications specific to repair of type B dissections include paraplegia/paraparesis (up to 40% with rupture), renal and intestinal ischemia, recurrent laryngeal nerve palsy, and chylothorax.45 Important late complications of both type A and type B dissections include late aneurysm formation and redissection of the aorta. In type B dissections moderate to severe aortic insufficiency is present late in 5% to 20% of patients with insufficiency preoperatively. This is usually well tolerated, with over 80% of these patients not requiring valve replacement at 10 years follow-up.46

Mortality

Acute type A dissections have an approximate mortality risk of 20% with operation (range = 7% to 35%). The risk is increased with rupture, age >80 years old, and associated illnesses, especially coronary artery diseases and preoperative hemodynamic instability.

Patients with type B dissections survive with medical therapy in 80% of cases. If complications arise requiring surgery, then the mortality increases, reaching 75% if renal and visceral artery occlusion is present.

Control of the patient's blood pressure and close observation for the development of late aneurysm are the most important variables determining the late complications and survival in type A and B dissections, whether they have undergone surgical repair or not.2,46,47 The development and rupture of postdissection aneurysms account for 30% of all late deaths. In the postoperative period, the systolic blood pressure is maintained at the lowest level capable of sustaining normal organ function, as indicated by sensorium, urine output, and other parameters. When the patient is transferred to the ward and onto oral antihypertensives, the type and dose must be modified to prevent orthostatic hypotension and syncope. Some form of β-blocker must be used (unless contraindicated) to control dP/dTmax as well as systolic pressure. The blood pressure control must be maintained lifelong so as to minimize the risk of late aneurysmal development or redissection.46 Follow-up must be performed regularly and over the long term, preferably with an easily available and reproducible imaging technique such as CT scanning.47 New aneurysms form because in 85% of cases the false lumen remains patent, and so the wall of the aorta is permanently weakened. DeBakey's study48 highlights the importance of long-term hypertension control. Five hundred twenty-seven patients were followed for 20 years after surgical repair of dissections. If hypertension was not controlled, 45.5% developed subsequent aneurysms, compared to 17.4% for those with proper control. Research is ongoing to improve stent-graft delivery and durability to improve long-term survival in these patients.49,50