Keywords
aortic dissection, surgical techniques
Step 1
Surgical Anatomy
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Type A dissection is defined by the presence of a septum creating two lumens within the ascending aorta. The DeBakey classification further divides the Stanford type A classification according to whether the septum is located solely in the ascending aorta (DeBakey type II) or extends distally within the arch and thoracoabdominal aorta (DeBakey type I; Fig. 24.1 ).
Figure 24.1
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The septum is secondary to an intimal tear, with separation of the media creating a true lumen—original aortic lumen lined by intima—and a false lumen, resulting from blood flow separating the media.
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In type A dissection, the primary intimal tear is located predominantly at the right anterolateral border of the ascending aorta, just above the sinotubular junction. In less than one-third of cases, the primary intimal tear may be located in the arch or thoracoabdominal aorta. In such cases, the septum in the ascending aorta is secondary to a retrograde extension of the dissection process.
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The dissection process may progress to the following:
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aortic rupture, usually within the pericardium
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extension to branch vessels such as the coronary ostia, arch vessels, and visceral arteries
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reentrance into the true lumen, with creation of reentry tears. Tears owing to the shearing of branch vessels of the aorta (natural fenestrations) also contribute to equilibrate the pressure between the true and false lumens.
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The dissection process often extends to the aortic root, with loss of commissural support of the aortic valve (mainly the left noncoronary commissure), and may lead to aortic valve malcoaptation and aortic insufficiency ( Fig. 24.2 ).
Figure 24.2
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Organ malperfusion secondary to branch vessel occlusion may supervene after type A dissection. The cause of the malperfusion may be dynamic or static ( Fig. 24.3 ).
Figure 24.3
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Dynamic branch vessel malperfusion is caused by high pressure within the false lumen, with collapse of the true lumen (see Fig. 24.3A ). True lumen branch vessels are hypoperfused because of proximal true lumen aortic collapse or ostial occlusion by the displaced septum. This represents the most frequent mechanism of malperfusion with type A dissection; it is usually relieved by successful reperfusion of the true lumen with operative repair.
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Static malperfusion is caused by occlusion of a branch vessel secondary to extension of the dissection process within the branch vessel (see Fig. 24.3B ). A branch vessel hematoma and reentry flap with in the branch vessel resulting in occlusion are examples. Malperfusion often persists following aortic repair.
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Combined malperfusion results from a combination of dynamic and static causes.
Step 2
Preoperative Considerations
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A diagnosis of acute type A dissection mandates an emergent operative procedure because historic reports have established that up to 1% to 2% of patients die each hour following the insult. Early medical therapy may lessen the risk of early rupture but still mandates emergent operative repair. Operative indications should be individualized in older patients with significant comorbidities or in patients with a severe neurologic deficit and a delayed presentation (> 6 hours) because operative mortality and morbidity rates are very high.
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Once the diagnosis is suspected, aggressive medical treatment should be instituted and diagnostic confirmation obtained, followed by operative repair:
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Pulse and dP/dt control using either beta blocker–/nitroprusside or a labetalol (Ttrandate) strategy
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Invasive monitoring
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Pain control
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Patients with severe malperfusion, such as visceral ischemia with an elevated lactate level, may initially be managed with an endovascular approach. This can be followed by an open aortic repair once the malperfusion is relieved and the patient is more stable.
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Although patients may be directed to the operating room solely on the visualization of a septum within the ascending aorta on transthoracic echocardiography, most patients are diagnosed by computed tomography (CT) angiography. This may provide additional information, such as extent of the dissection and involvement of branch vessels, site of the primary intimal tear, and the presence of pericardial effusion, malperfusion, and aneurysmal dilation.
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Coronary angiography is time-consuming and is usually not performed. However, patients with obvious signs of coronary malperfusion and hemodynamic compromise may initially be considered for coronary artery stenting, followed by definitive repair. Patients with a previous coronary artery bypass graft or who have known severe coronary artery disease may be considered for preoperative coronary angiography or cardiac coronary CT on a selected basis.
Step 3
Operative Steps
1
Anesthesia Preparation
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In addition to the standard monitoring during cardiac surgery, near-infrared spectroscopy (NIRS) may be of additional value to monitor brain saturation and differences between hemispheres during the circulatory arrest period.
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Temperature monitoring should include determining the nasopharyngeal, pulmonary artery, and bladder temperatures.
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Pharmacologic additives may be used. In preparation for circulatory arrest, mannitol, 0.5 g/kg, is administered to promote diuresis. The use of barbiturates such as pentobarbital or the use of corticosteroids remains controversial.
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Transesophageal echocardiography (TEE) is mandatory. The baseline evaluation includes assessment of myocardial function and the evaluation of pericardial effusion, aortic valve competency, site of the primary intimal tear, aortic diameters, and concomitant valvular problems. In addition, TEE is essential to monitor cardiopulmonary bypass (CPB)–induced malperfusion. Preferential perfusion of the true lumen should be assessed regularly, especially at critical time points such as CPB initiation, after aortic cross-clamping of the ascending aorta (if performed), and during resumption of CPB after the circulatory arrest period.
2
Cardiopulmonary Circuit Preparation
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The arterial line should be divided into two arms using a “Y” connector to reperfuse the distal aorta once the distal anastomosis is performed or to select an alternate cannulation site in case of malperfusion on CPB initiation.
3
Cardiopulmonary Initiation
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The femoral artery has been historically used as inflow during type A dissection. The right axillary artery has emerged as the preferred arterial cannulation site. The femoral artery, however, is rapidly accessible for hemodynamically unstable patients. The right axillary cannulation requires more time but ensures antegrade aortic perfusion, facilitates initiation of antegrade cerebral perfusion, and is associated with less malperfusion than the femoral artery.
Right Axillary Artery Cannulation Technique
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The right axillary artery dissection and cannulation are performed before sternal opening. Dissection of the axillary artery, a rare occurrence, is a contraindication to using the artery as arterial inflow. Dissection of the innominate artery, with or without extension in the proximal subclavian artery, is not a contraindication per se but is associated with a higher risk of malperfusion on CPB initiation.
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An infraclavicular incision is performed at the distal third of the clavicula. The fibers of the pectoralis major are divided, exposing the clavipectoral fascia, which is incised. The axillary artery lies posterior and cephalic to the axillary vein. Often, an arterial branch of the axillary artery lies in proximity to the border of the pectoralis minor and may be used to gain access to the axillary artery. The artery is looped with a Silastic tape. Systemic administration of 5-1000 U of heparin is given before vessel clamping. Cannulation may be carried out by inserting a cannula directly into the axillary artery or by sewing an 8-mm Dacron graft in an end-to- side fashion to the axillary artery. A 20 F cannula is then inserted into the graft and connected to one branch of the arterial line ( Fig. 24.4 ). Vascular complications are reported to be less with the 8-mm graft technique, especially in the presence of small axillary arteries.
