Surgical Therapy for Aortic Dissection

Morgagni described the first cases of aortic dissection in 1773, and Maunoir coined the entity “aortic dissection.” Despite these early reports of thoracic aortic disease, it was not until 1952 that Drs. De Bakey and Cooley first successfully operated on a patient with a descending thoracic aortic aneurysm using a lateral resection. In 1956 De Bakey and Cooley replaced the ascending aorta using cardiopulmonary bypass and homograft for conduit. Grafts manufactured from polyester cloth were later used as the preferred conduit for aortic replacement. The hemostatic qualities of synthetic grafts have been improved by modifications in textile engineering through the impregnation of collagen or gelatin. The routine use of cardiopulmonary bypass and widespread availability of synthetic graft material ushered in the modern era of surgical treatment for aortic dissection. Nevertheless, surgical management of aortic dissection remains a formidable challenge to surgeons. In addition to the inherent weak nature of the aortic tissues, patients may present with a wide spectrum of anatomic and physiologic derangements. Surgical decision making hinges on three primary considerations: (1) anatomic location of the dissection, (2) the time course in respect to onset of symptoms, and (3) the presence of complications related to the dissection.

The DeBakey and Stanford classifications define dissections according to their anatomical location; both systems place significance on involvement of the ascending aorta ( Fig. 33.1 ). DeBakey type I dissection originates in the ascending aorta and extends for a varying distance into the thoracoabdominal aorta, often reaching the aortic bifurcation. DeBakey type II dissection is limited to the ascending aorta. Type IIIa includes dissections with an origin in the descending thoracic aorta and no abdominal involvement. Type IIIb has origin in the descending thoracic aorta but includes abdominal extension. The Stanford system categorizes aortic dissection in two functional groups and is widely incorporated in clinical practice due to its simplicity. Any dissection involving the ascending aorta is categorized as type A, irrespective of the entry tear site or distal extent.

Timing of the operation in relation to onset of symptoms is important because surgical repair becomes safer as the dissection becomes older and the aorta less fragile. Risks posed by tissue fragility must be weighed against the competing risk of acute complications, which include rupture, severe aortic regurgitation, heart failure, and malperfusion. Although somewhat arbitrary, the Society of Thoracic Surgeons has differentiated timing of aortic dissection into the following categories: hyperacute (< 48 hours), acute (48 hours to 2 weeks), subacute (> 2 weeks to 90 days), and chronic (> 90 days).

Aortic dissections can cause numerous potentially lethal complications that warrant emergent surgical intervention. Aortic rupture can occur anywhere along the dissected aorta. Life-threatening proximal aortic complications include pericardial tamponade, acute aortic valve regurgitation, and myocardial infarction (MI) from coronary artery malperfusion. In more distal segments of the aorta, branch vessel malperfusion may lead to stroke, paraplegia, mesenteric ischemia, kidney failure, and limb-threatening ischemia ( Fig. 33.2 ). The combination of these potential complications with severe physiological derangements and extreme tissue fragility make aortic dissection one of the most formidable conditions treated by cardiovascular surgeons.

The three previously listed considerations form the basis for surgical intervention and operative strategies for aortic dissection. Surgical procedures to address proximal aortic dissections involving the ascending aorta and transverse aortic arch differ distinctly from strategies for treating distal aortic dissections involving the descending thoracic and thoracoabdominal aorta. Accordingly, type A and type B aortic dissection will be discussed independently.

Type a Aortic Dissection

Natural History

Elective aortic replacement in patients with ascending aortic aneurysm may prophylactically prevent aortic catastrophes such as acute type A aortic dissection, which harbors a very high mortality. The grim natural history of untreated acute type A aortic dissection is underscored by data reporting 50% mortality at 48 hours. However, recent studies have questioned the “1% mortality per hour” that has been previously associated with missed diagnoses or delayed treatment. In a study involving only octogenarians, 25% of patients were unfit to undergo surgery and successfully managed medically. Nevertheless, the extensive morbidity associated with acute type A dissection highlights the importance of prompt diagnosis and expedient surgical intervention in patients determined to be surgical candidates.

Indications for Operation

Aortic repairs for type A aortic dissection undertaken in the chronic phase invariably have superior results compared to those performed in the acute timeframe. Unfortunately, the high risk associated with early operation is outweighed by the even greater risk of a patient suffering a fatal complication (e.g., aortic rupture, coronary malperfusion) while undergoing medical management. Therefore, the presence of an acute type A aortic dissection has traditionally been considered an absolute indication for emergency surgical repair and remains the standard approach. Although controversial, delayed operative management of acute type A aortic dissection has been suggested for the following scenarios: elderly patients, patients with severe malperfusion, dissection occurring after prior cardiac surgery, and to enable transport to a specialized center.

Elderly Patients

Emergent repair of type A dissection in patients with advanced age greater than 80 years remains controversial. In recent literature, operative mortalities of nearly 50% have been reported for octogenarian patients. One may argue that surgical treatment is not warranted in the elderly because it does not alter the unfavorable natural history of the disease. In addition, while not reaching significance, an International Registry of Aortic Dissection (IRAD) study revealed an absolute survival benefit of 20% among elderly patients who underwent surgical repair of acute type A aortic dissection compared with medical management.

Surgical results of institutions and communities should be considered to optimize best outcomes. Extensive operations such as total arch or aortic root replacement should be weighed against the mortality risk associated with these prolonged and technically challenging operations. In patients whose compromised physiological reserve makes them poor candidates for emergency aortic repair, initial medical optimization followed by semielective surgery may be a reasonable treatment strategy.

Severe Malperfusion

Branch-vessel obstruction due to dissection may cause a wide spectrum of malperfusion syndromes ranging from mild (e.g., weakened distal extremity pulse) to severe (e.g., frank stroke or bowel infarction with necrosis) ( Box 33.1 ). In many cases of mild malperfusion, repair of the proximal aorta restores predominant flow through the true lumen and corrects distal malperfusion. However, patients in whom ischemia has caused severe end-organ dysfunction are unlikely to benefit from immediate ascending aortic repair. Stroke with resulting coma and bowel infarction with frank peritonitis remain ominous conditions in the setting of type A aortic dissection. Due to these observations, some centers advocate a strategy of delayed surgical treatment in patients with severe malperfusion. These strategies involve aggressive pharmacological treatment to reduce dP/dt (rate of rise of left ventricular [LV] pressure), diagnostic angiography, and percutaneous fenestration or stenting to augment true lumen flow to compromised branch vessels. Delayed proximal aortic operation is undertaken once the patient has recovered from the malperfusion. The optimal treatment strategy in these critically ill patients remains a topic of debate.

Box 33.1

Definitions of Severe Malperfusion

Severe Myocardial Malperfusion

Acute infarction diagnosed by electrocardiographic changes or elevated myocardial-specific enzyme levels associated with new-onset ventricular dysfunction

Severe Cerebral Malperfusion

Generalized nonresponsiveness or severe localized neurological deficit lasting > 48 h

Severe Visceral Malperfusion

Abdominal pain, physical findings consistent with an acute abdomen, and associated abnormal laboratory findings including lactic acidosis

Severe Extremity Malperfusion

New-onset absence of pulse for more than 4 h associated with pain, neurological symptoms, and physical findings consistent with threatened limb function

Modified from Deeb GM, Williams DM, Bolling SF, et al. Surgical delay for acute type A dissection with malperfusion. Ann Thorac Surg. 1997;64:1669–1675.

Type A Dissection After Prior Cardiac Surgery

Delayed management with elective operation has been proposed for patients who have had previous cardiac surgery. The presence of prosthetic aortic valves, aortic suture lines, coronary bypass grafts, and mediastinal adhesions surrounding the aortic wall are theoretically considered protective. Their presence can potentially prevent rupture, avoid valvular insufficiency, and minimize coronary malperfusion. In one study by the IRAD investigators, patients with type A aortic dissection and a history of previous cardiac operations were less likely to present with chest pain and cardiac tamponade than those without a history of previous cardiac operations. It should be emphasized that the perceived reduced rupture risk has not been conclusively supported by the available literature and does not apply to dissections occurring during the initial several weeks after cardiac surgery. Acute type A aortic dissection during the early postoperative period carries a high risk of rupture and tamponade; these patients should undergo early reoperation. Patients with ongoing chest pain should also undergo prompt surgical repair as well.

Transport to Specialized Centers

Patients with type A aortic dissections frequently require transport to centers where cardiac surgery services are available. Even in centers that offer cardiac surgery, transfer to high-volume centers may be considered in hemodynamically stable patients. There is evidence of improved outcomes in patients transferred to specialized centers. Prior to initiating transport, the patient's condition must be stabilized. Aggressive pharmacological management should be initiated and metabolic derangements addressed. Consistent administration and titration of vasoactive infusions during transport can be facilitated by central venous and arterial catheters. Inotropic agents and diuretic therapy can be given to patients presenting with low cardiac output and acute ventricular distention due to aortic valvular insufficiency and volume overload. If patients with pericardial tamponade must be transferred, a pericardial drain should be placed to allow intermittent drainage during transport. Whenever possible, patients with limb-threatening ischemia should undergo revascularization—usually via femoral-to-femoral artery bypass—before transport to minimize the severe metabolic derangements that result from prolonged limb ischemia and improve chances of survival. Standardized treatment protocols have been developed to optimize the hemodynamic management of patients with type A aortic dissection during transport.

Surgical Repair

Preoperative Considerations

There are several important considerations that may influence conduct of the operation, including the presence of connective tissue disorder, preexisting aortic root or arch aneurysm, and presence of severe malperfusion. A dissection that occurs in the setting of a preexisting aneurysm will likely require complete replacement of that segment. Preoperative computed tomography (CT) scans provide information about true lumen compression and existing malperfusion. Identification of which femoral vessel will provide access to the true lumen has implications for hemodynamic monitoring, cannulation for CPB, and subsequent access for revascularization procedures such as femoral-femoral bypass. The extent of aortic valve incompetence on preoperative echocardiography and any contraindications to anticoagulation will also dictate the need for aortic valve replacement and prosthesis type (mechanical vs. biological).

Cardiopulmonary Bypass

Median sternotomy provides access to the heart and proximal aorta. There are numerous options for arterial access to safely establish cardiopulmonary bypass. Peripheral options in cannulation for arterial inflow include the femoral artery and axillary artery. The femoral artery is a reliable option, which can provide rapid access in patients who are in extremis, although malperfusion and retrograde atheroembolization can occur. The axillary artery usually allows perfusion of true lumen and simplifies antegrade cerebral perfusion. Occasionally dissection may involve the innominate artery and extend into the axillary artery, and one should exercise extreme caution if deciding to cannulate this vessel. Central aortic cannulation, either via direct ascending aortic cannulation or advancement of the cannula into the ascending aorta via the LV apex, is a feasible alternative. Direct ascending cannulation is performed using Seldinger technique and is reliant on echocardiographic imaging to ensure wire access in the true lumen. Venous drainage is accomplished using a dual-stage cannula placed in the inferior vena cava (IVC) via the right atrium. Standard LV venting is performed with a vent catheter placed in the left ventricle via the right superior pulmonary vein.

Most surgeons perform type A aortic dissection repair utilizing a period of hypothermic circulatory arrest. This permits an open distal aortic anastomosis and the opportunity for visual inspection of the entire arch to ensure no additional intimal tears are present. Furthermore, this strategy avoids additional intima tears that may occur from an aortic clamp positioned across the fragile aorta.

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