A Practical Approach to Cardiac Anesthesia (Practical Approach Series) 5th Ed.

25 Anesthetic Management for Thoracic Aortic Aneurysms and Dissections

Amanda A. Fox and John R. Cooper, Jr.


 1. An aortic dissection usually occurs when blood penetrates the aortic intima, forming either an expanding hematoma within the aortic wall or simply a false channel for blood flow between the medial layer.

 2. An aortic aneurysm involves dilation of all three layers of the aortic wall.

 3. The term dissecting aneurysm, although commonly used, is often a misnomer because the aorta may not be dilated.

 4. Nitroprusside, a potent arterial dilator, and a β-blocker to decrease LV ejection velocity are critical to prevent further propagation of aortic dissection, rupture of a torn aorta, or leaking thoracic aortic aneurysm.

 5. Aortic valve repair or replacement is often needed with repair of aortic dissections or aneurysms. Which procedure is used depends on involvement of the sinus of Valsalva and the aortic annulus.

 6. Management of left heart bypass (LHB) can be very challenging for the cardiac anesthesiologist while repairing descending thoracic aneurysms or aortic tears (see Table 25.12). TEE is very useful to guide volume management, as native cardiac output must be preserved to provide adequate blood flow to the brain.

 7. Cerebral spinal drainage has been shown to significantly decrease postoperative paraplegia and paraparesis in a randomized controlled trial in patients undergoing descending thoracic surgery.

ANESTHESIOLOGISTS CARING FOR THORACIC AORTIC surgical patients encounter considerable variation between patients with regard to the cause and location of aortic disease. It is vital that anesthesiologists understand the implications of and the challenges related to these variations in providing optimal perioperative care. Members of both the American Society of Anesthesiologists and the Society of Cardiovascular Anesthesiologists were involved in the multidisciplinary development of the 2010 ACCF/AHA/AATS/ACR/ASA/SCA/SCAI/SIR/STS/SVM Guidelines for the Diagnosis and Management of Patients with Thoracic Aortic Disease [1]. This chapter gives a concise overview of the pathophysiology of thoracic aortic surgery, a review of its surgical approaches and results, and a rational approach to managing patients undergoing thoracic aortic surgery. Surgery on the thoracic aorta and, in particular, the descending and thoracoabdominal aorta may obviously involve complicated surgical and anesthetic management. Therefore, each team member must have a clear understanding of what is being planned. Often, all that is required is a brief preoperative conversation between the surgeon and the anesthesiologist as to the exact requirements for a particular procedure.


I. Classification and natural history

   A. Dissections. An aortic dissection usually occurs when blood penetrates the aortic intima, forming either an expanding hematoma within the aortic wall or simply a false channel for flow between the medial layers. (This expanding hematoma may be called a dissecting hematoma.) The true lumen of the dissecting aorta is generally not dilated; rather, it is often compressed by the dissection. Because the dissection does not necessarily involve the entire circumference of the aorta, branching vessels may be not affected, they may be occluded, or they may arise from the false lumen. In contrast, an aortic aneurysm involves dilation of all three layers of the aortic wall and has different pathophysiology and management concerns. The term dissecting aneurysm, although commonly used, is often a misnomer because the aorta may not be dilated.


     1. Incidence and pathophysiology


        a. Incidence. The incidence of dissection in the United States is unclear mainly because of under-reporting; however, European studies have reported an incidence of 3.2 dissections per 100,000 autopsies, with increasing numbers over time. Also, dissections resulted in more deaths than did aneurysm rupture [2].

        b. Predisposing conditions. The medical conditions predisposing to aortic dissection are listed in Table 25.1 in their order of importance. Interestingly, atherosclerosis by itself may not contribute to the risk of subsequent aortic dissection.

Table 25.1 Conditions predisposing to aortic dissections

        c. Inciting event. The onset of aortic dissections has been associated with increased physical activity or emotional stress. Dissections also have been associated with blunt trauma to the chest; however, the temporal relationship of blunt trauma and subsequent dissections has not been well established. Dissections can occur without any physical activity. They may also occur during cannulation for cardiopulmonary bypass (CPB), either antegrade from the ascending aorta or retrograde from the femoral artery.

        d. Mechanism of aortic tear. An intimal tear is the initial event in aortic dissection. The intimal tear of aortic dissections usually occurs in the presence of a weakened aortic wall, predominantly involving the middle and outer layers of the media. In this area of weakening, the aortic wall is more susceptible to shear forces produced by pulsatile blood flow in the aorta. The most frequent locations of intimal tears are the areas experiencing the greatest mechanical shear forces, as listed in Table 25.2. The ascending and isthmic (just distal to the left subclavian artery) segments of the aorta are relatively fixed and thus subject the aortic wall to the greatest amount of mechanical shear stress. This explains the high incidence of intimal tears in these areas.

Table 25.2 Sites of primary intimal tears in acute dissections

            In large autopsy series, however, up to 4% of dissections had no identifiable intimal disruption. In these cases, rupture of the vasa vasorum, the vessels that supply blood to the aortic wall, has been implicated as an alternative cause of dissections. The thin-walled vasa vasorum are located in the outer third of the aortic wall, and their rupture would cause the formation of a medial hematoma and propagation of a dissection in the presence of an already diseased vessel, without formation of an intimal tear.

        e. Propagation. Propagation of an aortic dissection can occur within seconds. The factors that contribute to propagation are the hemodynamic forces inherent in pulsatile flow: pulse pressure and ejection velocity of blood.

        f. Exit points. Exit points of dissections are found in a relatively small percentage of cases. Exit point tears usually occur distal to the intimal tear and represent points at which blood from the false lumen re-enters the true lumen. The presence or absence of an exit point does not appear to have an impact on the clinical course.

        g. Involvement of arterial branches. The origins of the major branches of the aorta, including the coronary arteries, may be involved in aortic dissections. Their involvement ranges from branch vessel occlusion via mechanical compression by the false lumen or from propagation of the dissecting hematoma into the arterial branch. The incidence of involvement of arterial branches gathered from a large autopsy series is listed in Table 25.3 [3].

Table 25.3 Involvement of major arterial branches in aortic dissections

     2. DeBakey classification of dissections (Fig. 25.1). This classification consists of three different types based upon the location of the intimal tear and which section of the aorta is involved.

Figure 25.1 DeBakey classification of aortic dissections by location: Type I, with intimal tear in the ascending portion and dissection extending to descending aorta; Type II, ascending intimal tear and dissection limited to ascending aorta; Type III, intimal tear distal to left subclavian, but dissection extending for a variable distance, either to the diaphragm (a) or to the iliac artery (b). (From DeBakey ME, Henly WS, Cooley DA, et al. Surgical management of dissecting aneurysms of the aorta. J Thorac Cardiovasc Surg. 1965;49:131, with permission.)

        a. Type I. The intimal tear is located in the ascending portion, but the dissection involves all portions (ascending, arch, and descending) of the thoracic aorta.

        b. Type II. The intimal tear is in the ascending aorta, but the dissection involves the ascending aorta only, stopping before the takeoff of the innominate artery.

        c. Type III. The intimal tear is located in the descending segment. If the dissection involves the descending portion of the thoracic aorta only, starting distal to the origin of the left subclavian artery and ending above the diaphragm, it is a Type III A. If the dissection propagates below the diaphragm, it is a Type III B. By definition, Type III dissections can extend proximally into the arch, but this is rare.

     3. Stanford (Daily) classification of dissections (Fig. 25.2). This classification is simpler than DeBakey’s and has more clinical relevance.

Figure 25.2 Stanford (Daily) classification of aortic dissections. Type A describes a dissection involving the ascending aorta regardless of site of intimal tear (1, ascending; 2, arch; 3, descending). In Type B, both the intimal tear and the extension are distal to the left subclavian. (From Miller DC, Stinson EB, Oyer PE, et al. Operative treatment of aortic dissections. Experience with 125 patients over a sixteen-year period. J Thorac Cardiovasc Surg. 1979;78:367, with permission.)

        a. Type A. Type A dissections are those that have any involvement of the ascending aorta, regardless of where the intimal tear is located and regardless of how far the dissection propagates. Clinically, Type A dissections run a more virulent course and are generally considered urgent or emergent cases.

        b. Type B. Type B dissections are those that involve the aorta distal to the origin of the left subclavian artery.

     4. Natural history

        a. Mortality—untreated. The survival rate of untreated patients with ascending aortic dissections is dismal, with a 2-day mortality of up to 50% in some series and 3-month mortality approaching 90% [3]. The usual cause of death is rupture of the false lumen into the pleural space or pericardium. Mortality is lower with DeBakey Type III or Stanford B dissections. Other causes of death include progressive cardiac failure (aortic valve involvement), myocardial infarction (coronary artery involvement), stroke (occlusion of cerebral vessels), and bowel gangrene (mesenteric artery occlusion).

        b. Surgical mortality. Overall mortality ranges from 3% to 24% and varies with the section of aorta that is affected. Dissections involving the aortic arch carry the highest mortality, while those confined to the descending thoracic aorta carry the lowest [2].

   B. Aneurysms

     1. Incidence. The European studies cited above report an incidence of thoracic aneurysms in approximately 460 autopsies per 100,000. In one study, 45% of thoracic aneurysms involved the ascending aorta, 10% the arch, 35% the descending aorta, and 10% the thoracoabdominal aorta [4].

     2. Classification by location and cause. In general, the causes and pathophysiology of aortic aneurysms are site dependent. Most commonly, medial degeneration affects the ascending aorta, while degenerative conditions associated with atherosclerosis affect the descending and thoracoabdominal portions of the aorta. Other causes are listed in Table 25.4.

Table 25.4 Causes of aneurysms based on location in the aorta

     3. Classification by shape

        a. Fusiform. Fusiform aneurysmal dilation involves the entire circumference of the aortic wall.

        b. Saccular. Saccular aneurysms involve only part of the circumference of the aortic wall. Isolated aortic arch aneurysms are commonly saccular.

     4. Natural history. The natural history of aortic aneurysms is one of progressive dilation, with more than half of aortic aneurysms eventually rupturing. The untreated, 5-yr rate of survival for patients with thoracic aortic aneurysms ranges from 13% to 39% [2]. Other complications of thoracic aortic aneurysms include mycotic infection, atheroembolism to peripheral vessels, and dissection. This last complication is rare, probably occurring in fewer than 10% of cases. Some predictors of poor prognosis are large size (greater than 10 cm maximum transverse diameter), presence of symptoms, and associated cardiovascular disease, especially coronary artery disease, myocardial infarction, or cerebrovascular accident.

   C. Thoracic aortic rupture (tear)

     1. Etiology. The overwhelming majority of thoracic aortic ruptures occur after trauma and almost always involve a deceleration injury from a motor vehicle accident. Sudden deceleration places large mechanical shear stress on points of the aortic wall that are relatively immobile. While aortic rupture leads to immediate exsanguination and death in many patients, approximately 10% to 15% of these patients maintain integrity of the adventitial covering of the aortic lumen and survive to emergency care. Surgical treatment of these survivors is often successful.

     2. Location. Most thoracic aortic ruptures occur just distal to the origin of the left subclavian artery (isthmus) because of the relative fixation of the aorta at this point by the ligamentum arteriosum (Fig. 25.3). The second most common site of aortic rupture is in the ascending aorta, just distal to the aortic valve.

Figure 25.3 The heart and great vessels are relatively mobile in the pericardium, whereas the descending aorta is relatively fixed by its anatomic relations. The attachment of the ligamentum arteriosum enhances this immobility and increases the risk of aortic tear due to deceleration injury. (From Cooley DA, ed. Surgical Treatment of Aortic Aneurysms. Philadelphia, PA: WB Saunders; 1986:186, with permission.)

II. Diagnosis

   A. Clinical signs and symptoms (Table 25.5)

Table 25.5 Presenting clinical signs and symptoms by location and type of aortic pathology

     1. Dissections. Aortic dissections usually present with a dramatic onset and a fulminant course. Clinical presentation of Stanford Types A and B are listed in Table 25.5.

     2. Aneurysms. Aneurysms of the ascending, arch, or descending thoracic aorta are often asymptomatic until late in their course. In many circumstances, the presence of an aneurysm is not diagnosed until medical evaluation is conducted for an unrelated problem or for a problem related to a complication of the aneurysm.

     3. Traumatic rupture. Ruptures most commonly occur just distal to the left subclavian artery. If the patient survives the initial trauma, signs and symptoms are similar to those seen with aneurysms of the descending thoracic aorta.

   B. Diagnostic tests

     1. Electrocardiogram (ECG). Many patients with aortic disease will have evidence of left ventricular (LV) hypertrophy on ECG, secondary to the high incidence of hypertension in these patients. In the setting of aortic dissection, the ECG may show ischemic changes caused by coronary artery involvement or evidence of pericarditis from hemopericardium.

     2. Chest X-ray film. A widened mediastinum is a classic X-ray finding with thoracic aortic pathology. Widening of the aortic knob is often seen, with disparate ascending-to-descending aortic diameter. A double shadow has been described in the setting of aortic dissection, secondary to visualization of the false lumen.

     3. Serum laboratories. There are no laboratory findings specifically found with asymptomatic aortic aneurysms. Aortic dissections or ruptures will decrease hemoglobin. Dissections may cause elevated cardiac enzymes from coronary artery occlusion, may increase blood urea nitrogen and creatine from renal artery involvement, and may lead to metabolic acidosis from low cardiac output or ischemic bowel. Fibrinogen may decrease in patients experiencing associated disseminated intravascular coagulation.

     4. Computed tomographic (CT) scans and magnetic resonance imaging. CT is a useful tool for ascertaining aneurysm size and location and has replaced angiography in many instances. It is also useful for following the progression of aortic disease. Digital images can be manipulated into a three-dimensional form, which may make it easier to assess the lesion and plan repair. Magnetic resonance imaging is extremely sensitive and specific in identifying the entry tear location, presence of false lumen, aortic regurgitation, and pericardial effusion accompanying aortic dissections [5].

     5. Angiography. This technique remains useful for determining the severity and extent of aortic aneurysms and dissections. With dissections it can be used to locate the site of an intimal tear, to assess aortic valve integrity, and to identify the distal and proximal spread. It can especially delineate involvement of the coronary arteries, as well as the presence of significant coronary artery disease in patients with ascending aortic pathology. Patients with disease of the thoracic aorta often have concurrent coronary artery disease, and bypassing significant lesions helps prevent perioperative myocardial infarction and improves ventricular function when weaning from CPB. Aortography can also determine if other major branch arteries off the aorta are involved. Unfortunately, aortography only rarely identifies those intercostal vessels that are critical for providing blood supply to the spinal cord (see Section IV.G).

     6. Transesophageal echocardiography (TEE). TEE has been found to be highly sensitive and specific for diagnosing aortic dissection. In many cases, pulsed-wave and color-flow Doppler imaging can aid in defining the presence, extent, and type of dissection. Identification of a mobile intimal flap provides a prompt bedside diagnosis that can be lifesaving. In addition, entry and re-entry tears can be defined; aortic regurgitation can be identified and quantified; assessment of LV function and wall motion abnormalities can be made; presence of pericardial effusion with possible associated cardiac tamponade can be identified; and follow-up studies of the false lumen can be made after therapeutic intervention.

          TEE can also be used to assess many thoracic aortic aneurysms. For ascending or descending thoracic aortic aneurysms in particular, the location, diameter, and extent of the aneurysm, as well as whether the aneurysm contains significant atheroma, can often be well described. TEE can also be used to determine if the aneurysm is saccular or fusiform in shape. TEE can be rarely used to define definitive aneurysmal involvement of the aortic arch and distal ascending aorta. This is because the trachea obscures the latter section from transesophageal ultrasound imaging and the entire arch is not usually visible on TEE. If the surgeon desires detailed preoperative imaging of the aortic arch, he or she should confer with a radiologist about magnetic resonance or CT imaging.

          Because traumatic aortic transection generally occurs just distal to the left subclavian takeoff, it is often easily and rapidly identified by TEE imaging. In addition, aortic transection operations are usually emergencies, so TEE imaging is advantageous because it can be conducted quickly and in most locations.

     7. Recommendation for diagnostic strategies. In hemodynamically stable patients, Nienaber and colleagues recommend diagnosis of thoracic aortic dissection noninvasively via magnetic resonance imaging because of its high degree of sensitivity (98.3%) and specificity (97.8%) [6]. For patients too unstable for this rather lengthy procedure (40 to 45 min), TEE, which has an average duration of about 15 min and a sensitivity and specificity of 97.7% and 76.9%, respectively, is recommended. Because of its general inability to provide additional information to that provided by more noninvasive methods and its higher incidence of complications, aortography is only useful in very select cases.

   C. Indications for surgical correction

     1. Ascending aorta

        a. Dissections. Acute Type A dissections should be surgically corrected, given their virulent course and high mortality if not surgically treated.

        b. Aneurysms. Indications for surgical resection include the following:

           (1) Presence of persistent pain despite a small aneurysm

           (2) Aortic valve involvement producing aortic insufficiency

           (3) Presence of angina from LV strain secondary to aortic valve involvement or from coronary artery involvement by the aneurysm

           (4) Rapidly expanding aneurysm or an aneurysm greater than 5 to 5.5 cm in diameter, because the chance of aortic rupture increases as the aneurysm’s size increases

     2. Aortic arch

        a. Dissections. Acute dissection limited to the aortic arch is rare but is an indication for surgery.

        b. Aneurysms. Since even elective surgical treatment of arch aneurysms is more difficult than surgery for other aortic aneurysms and is associated with a higher morbidity and mortality, management may be more conservative. However, arch involvement is often seen with ascending aneurysms (less so with descending aneurysms) and is dealt with during surgical repair of these lesions. Surgical indications include the following:

           (1) Persistent symptoms

           (2) Aneurysm greater than 5.5 to 6 cm in transverse diameter

           (3) Progressive aneurysmal expansion

     3. Descending aorta

        a. Dissection. Some controversy remains concerning the best treatment for an acute Type B dissection. Because of similar in-hospital mortality statistics for medical versus surgical interventions [7], Type B dissections are often treated medically in the acute phase, especially if the patient’s comorbidities make the chance of surgical mortality prohibitively high. However, patients with Type B dissections who have the following complications are treated surgically:

           (1) Failure to control hypertension medically

           (2) Continued pain (indicating progression of the dissection)

           (3) Enlargement on chest X-ray film, CT scan, or angiogram

           (4) Development of a neurologic deficit

           (5) Evidence of renal or gastrointestinal ischemia

           (6) Development of aortic insufficiency

            Note, as shown in Table 25.6, that the 10-yr survival of patients receiving medical management only for Type B dissections is slightly better than the combined survival of patients treated surgically for Type A and B dissections [7].

Table 25.6 Surgical versus medical therapy for aortic dissections

        b. Aneurysm. Indications for surgical repair of descending thoracic aneurysms include the following:

           (1) Aneurysm greater than 5 to 6 cm in diameter

           (2) Aneurysm expanding

           (3) Aneurysm leaking (more fulminant symptoms)

           (4) Chronic aneurysm causing persistent pain or other symptoms

III. Preoperative management of patients requiring surgery of the thoracic aorta.

Emergency preoperative management of aortic dissections is discussed below. However, emergency preoperative management is similar for a leaking thoracic aortic aneurysm or a contained thoracic aortic rupture .

   A. Prioritizing: Making the diagnosis versus controlling blood pressure (BP). In the setting of a suspected aortic dissection, aortic tear, or leaking aortic aneurysm, the first priority is always to control the BP and ventricular ejection velocity, as these propagate aortic dissection or rupture. If dissection is strongly suspected, making a definitive diagnosis with radiographic studies should occur after proper monitoring, intravenous (IVaccess, hemodynamic stability, and heart rate and BP control have been established (if possible). During diagnostic procedures, the patient should be monitored closely, with a physician present as clinically indicated. An anesthesiologist should become involved as early as possible, if needed, to lend expertise in monitoring and airway and hemodynamic management in cases where clinical deterioration occurs before the patient reaches the operating room. Rapid diagnosis using TEE may save critical minutes in initiating definitive surgical treatment in patients with suspected thoracic aortic dissection or rupture.


   B. Achieving hemodynamic stability and control. The ideal drug to control BP is administered by IV and is rapidly acting with a short half-life and few, if any, side effects. Systolic and diastolic BPs and LV ejection velocity should be reduced, because all these factors can propagate aortic dissection.

     1. Monitoring. Patients must have an ECG for detection of ischemia and dysrhythmias, two large-bore IV catheters for volume resuscitation, an arterial line in the appropriate location (discussed below), and, if time permits, a central venous catheter or pulmonary artery (PA) catheter for monitoring filling pressures and infusing drugs centrally.

     2. BP-lowering agents

        a. Vasodilators

           (1) Nitroprusside has emerged as a useful agent for controlling BP in patients with critical aortic lesions, because its rapid onset and offset make it quickly effective and easily regulated. A vasodilator that relaxes both arterial and venous smooth muscle, it is given as an IV infusion, and while central administration is probably optimal, it can be administered through a peripheral vein with good effect. The usual starting dose is 0.5 to 1 μg/kg/min, titrated to effect. Doses of 8 to 10 μg/kg/min have been associated with cyanide toxicity (see Chapter 2).

           (2) Nitroglycerin is a less potent vasodilator than sodium nitroprusside, and it causes more venous than arterial dilation. It can be useful in settings where ascending aortic pathology is coupled with myocardial ischemia, as it can improve coronary blood flow via coronary artery vasodilation. Infusion dosage usually ranges from 1 to 4 μg/kg/min.

           (3) Fenoldopam is a rapidly acting vasodilator that is a selective D1 dopamine receptor agonist. It has little affinity for the D2α1, or β adrenoreceptors. Fenoldopam causes vasodilation in many vascular beds, but it increases renal blood flow to a significant degree. Therefore, it may have some renal protective effects while also being used to treat acute hypertension. Dosing starts at 0.05 to 0.1 μg/kg/min and can be increased incrementally to a maximum dose of 0.8 μg/kg/min.

           (4) Nicardipine is a calcium-channel blocker that inhibits calcium influx into vascular smooth muscle and the myocardium. It may be used as a single 0.5 to 2 mg IV “push” or as a 5 to 15 mg/hr infusion titrated to the desired effect.

        b. b1-antagonists

            Decreasing LV ejection velocity is important for decreasing risk of propagating aortic dissection. Medications to lower heart rate may be particularly useful for attenuating reflex tachycardia and increased ventricular contractility that can occur with use of sodium nitroprusside. Nitroprusside can increase LV ejection velocity by increasing dP/dt and heart rate. For this reason, β -adrenergic blockade should be used with nitroprusside to decrease both tachycardia and contractility (see Chapter 2).

           (1) Propranolol, a nonselective β -antagonist, has been used for many years as first-line therapy for this role and can be administered as an IV bolus of 1 mg, but doses of 4 to 8 mg may be required for adequate heart rate control. Propranolol has been somewhat supplanted by selective β1-antagonists.

           (2) Labetalol is a combined α- and β-blocker and offers an alternative to the nitroprusside–propranolol combination. It should be given initially as a 5 to 10 mg loading bolus; once the effect has been assessed, the dose is doubled, allowing a few minutes for onset of effect. This process should be repeated until target BP or a total dose of 300 mg is reached. Once target BP and heart rate are achieved via the loading dose, a continuous infusion may be started at 1 mg/min, or a small bolus dose can be repeated every 10 to 30 min to maintain BP control.

           (3) Esmolol is a β-blocking agent with a short half-life that may be useful in this setting. It is administered as a bolus loading dose of 500 μg/kg over 1 min and then continued as an infusion starting at 50 μg/kg/min and titrated to effect to a maximum dose of 300 μg/kg/min. This drug is particularly useful in patients with obstructive lung disease because it is β1 selective and its action can be terminated quickly if β2-mediated respiratory symptoms ensue.

           (4) Metoprolol, another β1-selective agent, is used in doses of 2.5 to 5 mg titrated to effect over a few minutes to a maximum dose of 15 to 20 mg. It provides a longer effect, which may be useful.

     3. Desired endpoints. In order to decrease the chance of propagating aortic dissection or rupture, systolic BP should usually be lowered to approximately 100 to 120 mm Hg or to a mean pressure of 70 to 90 mm Hg. Heart rate should be 60 to 80 beats/min. If a PA catheter is in place, the cardiac index may be lowered to a range of 2 to 2.5 L/min/m2 to reduce ejection velocity from a hyperdynamic LV.

   C. Bleeding and transfusion. Coagulopathy is frequently encountered in the thoracic aortic surgical patient. Many of these patients require left heart or full CPB during surgery to help maintain sufficient end-organ perfusion during aortic repair; thus, they also require heparinization. CPB may cause a consumptive coagulopathy and enhanced fibrinolysis, thus increasing blood loss [8,9]. Patients requiring deep hypothermic circulatory arrest (DHCA) for aortic arch surgery also may experience substantial platelet dysfunction secondary to extreme hypothermia. Platelet consumption has also been noted in the abdominal aortic surgical population [10]. In patients undergoing thoracoabdominal aortic aneurysm repairs, “back-bleeding” through intercostal vessels increases blood loss, and very large losses necessitating transfusion of multiple units of blood products can occur [11].

      1. A total of 8 to 10 units of packed red blood cells should be typed and cross-matched before surgery.

      2. Use of blood scavenging/reprocessing devices decreases the amount of banked blood transfused, but extensive bleeding and the logistics of effectively scavenging autologous blood during these operations may frequently require transfusion of packed cells and procoagulant blood products.

      3. Antifibrinolytic therapy during aortic surgery is controversial but commonly used. Few adequately powered trials have examined this surgical population, so it is unclear if significant benefit is derived from antifibrinolytics, particularly in patients in whom left heart bypass (LHB) is used and full heparinization is unnecessary [12].

        a. Tranexamic acid or -aminocaproic acid. A retrospective study of 72 patients who underwent descending thoracic aortic surgery with LHB and tranexamic acid or -aminocaproic acid infusion versus no antifibrinolytic therapy found no difference in incidence of transfusion or chest tube output; however, all of these patients also received intraoperative methylprednisolone and platelet-rich plasmapheresis before aortic repair [12]. These authors did find that intraoperative hypothermia independently predicted chest tube output and that preoperative hemoglobin, older age, and duration of cross-clamp time independently predicted transfusion. Casati and colleagues conducted a single-institution, double-blind, randomized, controlled study of 60 consecutive elective thoracic aortic surgical patients, half of whom received perioperative tranexamic acid and the other half received a normal saline placebo [13]. This study found that the tranexamic acid recipients required significantly fewer packed red blood cell transfusions, as well as overall allogeneic transfusions, than the placebo recipients. No differences in perioperative thrombotic complications were noted between the tranexamic acid intervention group and the placebo group. However, this was a small study that was not statistically powered to evaluate the occurrence of adverse perioperative thrombotic events. Larger prospective randomized studies are needed to determine whether tranexamic acid or -aminocaproic acid effectively reduce bleeding and do not cause thrombotic complications in thoracic aortic operations, because there are no other data regarding the risk/benefit of these agents in thoracoabdominal aortic surgical patients.

        b. On the basis of available data, the authors can neither recommend nor advise against the use of antifibrinolytic therapies in thoracic aortic surgery. Potential thrombotic risks, including neurocognitive and renal dysfunction, are of concern, and the clinician should weigh these risks against the benefits of potential decreases in transfusion.

   D. Assessment of other organ systems

     1. Neurologic. Preoperatively the patient should be monitored closely for change in neurologic status, as this is an indication for immediate surgical intervention. Involvement of the artery of Adamkiewicz may lead to lower extremity paralysis, while propagation of a dissection into a cerebral vessel may lead to a change in mental status or stroke symptoms.

     2. Renal function. Urine output should be monitored, as development of anuria or oliguria in the euvolemic setting is an indication for immediate surgical intervention.

     3. Gastrointestinal. Serial abdominal examinations should be performed, and blood gas analysis should be done routinely to assess changes in acid–base status. Ischemic bowel can cause significant metabolic acidosis.

   E. Use of pain medications. Patients with aortic dissections may be anxious and in severe pain. Not only is pain relief important for patient comfort, but it is beneficial in controlling BP and heart rate. Oversedation should be avoided so that ongoing patient assessments may occur. In addition to neurologic or abdominal symptoms, worsening of back pain may indicate aneurysm expansion or further aortic dissection and is regarded by many surgeons as an emergent situation.

IV. Surgical and anesthetic considerations

   A. Goal of surgical therapy (for aortic dissections, aneurysms, or rupture). The foremost goal in treating acute aortic disruption is to control hemorrhage. Once control is achieved, the objectives of management of both acute and chronic lesions are to repair the diseased aorta and restore its relationships with major arterial branches.

       Thoracic aortic aneurysm repair is usually conducted by replacing the diseased segment of the aorta with a synthetic graft and then reimplanting major arterial branches into the graft. In contrast, when repairing an aortic dissection the goal is to resect the segment of the aorta that contains the intimal tear. When this segment is removed, it may be possible to obliterate the false lumen and interpose graft material. It is usually not possible or necessary to replace the entire dissection portion of aorta, because, if the origin of dissection is controlled, re-expansion of the true lumen usually compresses and obliterates the false lumen. With contained aortic rupture, the objective is to resect the area of the aorta that ruptured and either reanastomose the natural aorta to itself in an end-to-end fashion or interpose graft material for the repair.

   B. Overview of intraoperative anesthetic management (for aortic dissections, aneurysms, or rupture)

     1. Key principles

        a. Managing BP. BP control should be sought during the transition from the preoperative to the intraoperative period. Such control is important in light of the surgical and anesthetic manipulations that will profoundly affect BP.

        b. Monitoring of organ ischemia. If possible, the central nervous system, heart, kidneys, and lungs should be monitored for adequacy of perfusion. The liver and gut cannot be monitored continuously, but their metabolic functions can be checked periodically.

        c. Treating coexisting disease. Patients with aortic pathology often have associated cardiovascular and systemic diseases, as outlined in Table 25.7.

Table 25.7 Incidence of coexisting diseases in patients with aortic pathology

        d. Controlling bleeding. Patients undergoing aortic surgery often experience an inflammatory response to foreign graft material and cardiopulmonary or LHB. This inflammation can interact with the coagulation cascade and lead to significant perioperative coagulopathy. Furthermore, patients with acute dissection and lower fibrinogen and platelet counts may already have a consumptive process from the clotting that often occurs in the false lumen. The challenges of coagulation abnormalities and their treatment are discussed in Chapter 19.

     2. Induction and anesthetic agents. Many thoracic aortic operations are emergent procedures that require aspiration precautions when securing the airway. However, rapid sequence induction and intubation typically done for patients with full stomachs may not be appropriate for the patient with thoracic aortic pathology, as wide swings in hemodynamics may occur. A compromise in this situation is a smooth, controlled IV induction, with gentle manual ventilations and cricoid pressures held. This “modified” rapid sequence induction allows not only some airway protection but also titration of anesthetic induction drugs that control BP with laryngoscopy. Use of nonparticulate antacids, H2-blockers, and metoclopramide should be considered before induction of anesthesia. Other anesthetic considerations and agents are described more fully in Section IV.D. Despite precautions, marked changes in hemodynamics are common when securing the patient’s airway, and vasoactive drugs (nitroglycerin, esmolol, or others) should be available to immediately treat an undesirable hemodynamic response to intubation [14].

     3. Importance of site of lesion (Table 25.8). Although the principles of anesthetic induction and maintenance are similar for all aortic lesions, the location of the thoracic aortic lesion is also important for intraoperative management.

Table 25.8 Anesthetic and surgical management for thoracic aortic surgery

   C. Ascending aortic surgery

     1. Surgical approach. Ascending aortic surgery is conducted through a midline sternotomy.

     2. CPB. CPB is required because of proximal aortic involvement.

        a. If the aneurysm ends in the proximal portion or midportion of the ascending aorta, the arterial cannula for CPB can be placed in the upper ascending aorta or proximal arch.

        b. If the entire ascending aorta is involved, the femoral artery may be cannulated, because an aortic cannula cannot be placed distal to the lesion without jeopardizing perfusion to the great vessels. Arterial flow on CPB in this case is retrograde from the femoral artery toward the great vessels. Another, newer approach is to cannulate the right axillary, the innominate, or occasionally the right carotid artery, allowing retrograde perfusion into the innominate artery and then into the aorta in an antegrade manner.

        c. Venous cannulation is usually through the right atrium; however, femoral venous cannulation may be necessary if the aneurysm is very large and obscures the atrium.

     3. Aortic valve involvement. Aortic valvuloplasty or valve replacement is often needed with repair of ascending aortic dissections or aneurysms. Which procedure is used depends on the degree of involvement of the sinus of Valsalva and the aortic annulus.


     4. Coronary artery involvement. Ascending aortic dissections or aneurysms may involve the coronary arteries. Aortic dissections may cause coronary occlusion by compression of the coronary ostia by an expanding false lumen; such occlusion will require surgical coronary artery bypass grafting to restore myocardial blood flow. Displacement of the coronary arteries from their normal position distal to the aortic annulus with proximal aortic aneurysms usually requires coronary artery reimplantation into the reconstructed aortic tube graft or coronary artery bypass grafting.

     5. Surgical techniques. An example of the usual cross-clamp placement used in surgery of the ascending aorta is shown in Figure 25.4. Note that placement of the distal clamp is more distal than when cross-clamping for coronary artery bypass surgery and might include a part of the innominate artery. If aortic insufficiency is present, a large portion of the cardioplegic solution infused into the aortic root will flow through the incompetent aortic valve and into the LV instead of the coronary arteries. This can cause distention of the LV with increased myocardial oxygen utilization and diminished myocardial protection from reduced distribution of cardioplegia. For these reasons, an immediate aortotomy is often performed after aortic cross-clamping with direct infusion of cardioplegia into individual coronary arteries. Many centers also use retrograde coronary perfusion for cardioplegia administration as an alternative or in addition to an antegrade technique.

Figure 25.4 Circulatory support and clamp placement for surgery of the ascending aorta if femoral arterial cannulation is used; the distal clamp must be distal to the diseased segment. This may be the only clamp required. CPB, cardiopulmonary bypass. (From Benumof JL. Intraoperative considerations for special thoracic surgery cases. In: Benumof JL, ed. Anesthesia for Thoracic Surgery. Philadelphia, PA: WB Saunders; 1987:384, with permission.)

          If the aortic valve and annulus are both normal size and unaffected by concurrent ascending aortic pathology, surgery is limited to replacing the diseased section of the aorta with graft material. If the annulus is normal size, but the aortic valve is incompetent, the valve may be resuspended or replaced. If both aortic insufficiency and annular dilation are present, either a composite graft (i.e., a tube graft with an integral artificial valve) or an aortic valve replacement with a graft sewn to the native annulus can be used. The coronary arteries must be reimplanted into the wall of a composite graft, but they may not need to be reimplanted if separate aortic valve replacement and aortic tube grafts are used for the repair and the native sinus of Valsalva can be left in place (Fig. 25.5) [15]. The posterior wall of the native aneurysm can be wrapped around the graft material and sewn in place to help with hemostasis.

Figure 25.5 Surgical repair of ascending aortic aneurysm or dissection. A: Aortic valve has been replaced and the aorta is transected at native annulus, leaving “buttons” of aortic wall around coronary ostia. B: Graft material anastomosed to the annulus, with left coronary reimplantation. C: Completion of left and beginning of right coronary reimplantation. D: Completion of distal graft anastomosis. (From Miller DC, Stinson EB, Oyer PE, et al. Concomitant resection of ascending aortic aneurysm and replacement of the aortic valve—operative results and long-term results with “conventional” techniques in ninety patients. J Thorac Cardiovasc Surg. 1980;79:394, with permission.)

          In patients with ascending dissections, the aortic root is opened and the site of the intimal tear is located. The section of the aorta that includes the intimal tear is excised, and the edges of the true and false lumens are sewn together. Graft is used to replace the excised portion of the aorta.

     6. Complications. Complications include any that can occur with an operation involving CPB and an open ventricle:

        a. Air emboli

        b. Atheromatous or clot emboli

        c. LV dysfunction secondary to difficult myocardial protection during aortic cross-clamping

        d. Myocardial infarction or myocardial ischemia secondary to technical problems with reimplantation of the coronaries

        e. Renal or respiratory failure

        f. Coagulopathy

        g. Hemorrhage, especially from suture lines, which can be especially difficult to control

   D. Anesthetic considerations for ascending aortic surgery

     1. Monitoring

        a. Arterial line placement. The ascending aortic lesion or procedures for its repair may involve the innominate artery, so a left radial or femoral arterial line is inserted for direct BP monitoring. Also, if right axillary cannulation is used, arterial pressure measurements will be falsely elevated because of increased flow (see below).

        b. ECG. Five-lead, calibrated ECG should be used to monitor both leads II and V5 for ischemic changes.

        c. PA catheter. Because of the advanced age of many of these patients and the presence of severe systemic disease that may lead to pulmonary hypertension or low cardiac output, a PA catheter may be useful in selected patients in the perioperative period.

        d. TEE. In addition to its preoperative diagnostic importance, TEE is a useful adjunct for the intraoperative management of these patients. Hypovolemia, hypocontractility, myocardial ischemia, intracardiac air, the location of an intimal tear, and the presence and extent of valvular dysfunction can all be detected with TEE. Caution should be exercised when placing this probe in the presence of a large ascending aortic aneurysm because of theoretical risk of rupture.

        e. Neuromonitoring

           (1) Electroencephalogram (EEG). Either raw or processed EEG data may be helpful for judging the adequacy of cerebral perfusion during CPB. Monitoring the bispectral index might help to assess the depth of anesthesia during these procedures, but the benefits of such monitoring are unproven.

           (2) Temperature. When correctly placed at the back of the oropharynx, a nasopharyngeal or oropharyngeal temperature probe probably gives the anesthesiologist the best overall approximation of brain temperature.

        f. Renal monitoring. As with all cases involving CPB, urine output should be monitored.

     2. Induction and anesthetic agents. See Table 25.9.

Table 25.9 Anesthetic considerations and choice of anesthetic agent for surgery of the aorta

     3. Cooling and rewarming. Hypothermic CPB is used in most cases of ascending aneurysms. DHCA is needed if the proximal arch is involved. If femoral cannulation is used and the femoral artery is small, a smaller cannula may be needed. This may delay cooling and rewarming, because lower blood flows on CPB will have to be used to avoid excessive arterial line pressures between the roller pump and the arterial cannula.

   E. Aortic arch surgery

     1. Surgical approach. The arch is exposed through a median sternotomy.

     2. CPB. In most cases, CPB with femoral or right axillary arterial and right atrial venous cannulation is required.

     3. Technique. Typical aortic clamp placement for this procedure is shown in Figure 25.6. Note that blood flow to the innominate, left carotid, and left subclavian arteries will cease during resection of the aneurysmal or dissected section of the aortic arch, thus necessitating DHCA.

Figure 25.6 Representation of cannula and clamp placement for surgery of the aortic arch if femoral bypass is used. Proximal clamp is placed to arrest the heart. Distal clamp isolates the arch so that the distal anastomosis can be performed. Middle clamp on major branches isolates the head vessels so that en bloc attachment to graft is possible. The distal and arch anastomoses may be performed without clamps by using circulatory arrest. CPB, cardiopulmonary bypass. (From Benumof JL. Intraoperative considerations for special thoracic surgery cases. In: Benumof JL, ed. Anesthesia for Thoracic Surgery. Philadelphia, PA: WB Saunders; 1987:384, with permission.)

          The attachments of the arch vessels are usually excised en bloc so that all three vessels are located on one “button” of tissue, as shown in Figure 25.7 [16]. This facilitates rapid reimplantation and re-establishment of blood flow through the arch vessels. Once the distal arch anastomosis is completed, the surgeon sutures the aortic button containing the arch vessels to the graft that is replacing the diseased aortic arch. The aortic cross-clamp can then be placed on the graft proximal to the arch vessels, after which the arch portion of the aortic graft is deaired, and blood flow is re-established to the cerebral vessels via the arterial CPB cannula. The proximal aortic arch anastomosis is then completed.

Figure 25.7 Aortic arch replacement. A: The distal suture line is completed first, followed by (B) reattachment of the arch vessels. C: Flow is re-established to these vessels by moving the clamp more proximally. D: The proximal suture line is completed. (From Crawford ES, Saleh SA. Transverse aortic arch aneurysm—improved results of treatment employing new modifications of aortic reconstruction and hypokalemic cerebral circulatory arrest. Ann Surg. 1981;194:186, with permission.)

     4. Cerebral protection. As discussed above, resection of the aortic arch requires interruption or alteration of cerebral blood flow, which may contribute to postoperative stroke and neurocognitive dysfunction—both significant causes of morbidity and mortality in patients undergoing aortic arch surgery. Although various surgical approaches are used to reduce cerebral ischemia, all include lowering patient temperature with CPB in order to decrease the cerebral metabolic rate, the corresponding oxygen demand, and the production of toxic metabolites.

        a. DHCA is used for arch surgery, because blood flow through the aorta to the brain can be stopped and surgical exposure is maximized. DHCA requires cooling the patient’s core temperature to 15 to 22°C, depending on the anticipated complexity and duration of the procedure and the adjunctive technique used (antegrade cerebral perfusion [ACP] or retrograde cerebral perfusion [RCP]). Turning off CPB and partially draining the patient’s blood volume into the venous reservoir provides a bloodless surgical field, with effective protection of the brain and other organs, such as the kidneys, for 40 min [17], or perhaps longer. DHCA has improved outcomes for aortic arch surgery but is associated with longer CPB times to adequately cool and rewarm the patient. Animal studies suggest that it is important to rewarm patients relatively slowly after DHCA, and also not to rewarm the brain above 37°C, because this may cause increased cerebral injury [18]. Because of the limited time that patients can undergo DHCA before suffering cerebral injury, some surgeons use either selective retrograde perfusion or ACP as an adjunct to DHCA to prolong the “safe time” allowed for complicated reconstruction of the aortic arch and its branch vessels while circulation to the rest of the body is stopped.

        b. RCP does necessitate individual caval cannulation. At circulatory arrest, the arterial line of the CPB circuit is connected to the superior vena cava cannula and low flows are directed through the cannula to maintain a central venous pressure (CVP) of around 20 mm Hg [19], although this pressure is not necessarily associated with improved outcomes. Advantages of RCP include relative simplicity, uniform cerebral cooling, efficient deairing of the cerebral vessels (thus reducing the risk of embolism), and provision of oxygen and energy substrates. Outcome studies have identified the following risk factors for mortality and morbidity in RCP during DHCA: time on CPB, urgency of surgery, and patient age [20]. Controversy exists as to how much flow is actually directed to the brain and how much flow courses through the extracranial vessels.

        c. ACP. With this technique, the brain is selectively perfused via the innominate or carotid arteries [19]. As shown in Figure 25.8, one method for administering ACP is to take blood from the CPB circuit’s oxygenator and to deliver it via arterial access to the brain by using a separate roller pump from the one used for CPB [21]. Many centers use this same technique to deliver antegrade or retrograde cardioplegia.

Figure 25.8 Perfusion circuit for anterograde cerebral perfusion for aortic arch surgery. Venous blood from the right atrium drains to the oxygenator (Ox) and is cooled to 28°C by heat exchange (E2) before passing via the main roller pump (P2) to a femoral artery. A second circuit derived from the oxygenator with a separate heat-exchanger (E1) and roller pump (P1) provides blood at 6 to 12°C to the brachiocephalic and coronary arteries. (From Bachet J, Guilmet D, Goudot B, et al. Antegrade cerebral perfusion with cold blood: A 13-year experience. Ann Thorac Surg. 1999;67:1875, with permission.)

            Figure 25.8 [21] depicts direct cannulation of both carotid arteries for ACP, but this technique has been simplified in many practices by cannulating the right axillary artery or other arteries, as discussed above, for placement of the arterial line from the CPB circuit instead of using the femoral artery. This is usually done by anastomosing (side-to-end) a tube graft to the axillary artery and attaching the arterial line from the pump to the graft. After the patient is placed on CPB and cooled, at the time of circulatory arrest the base of the innominate artery is clamped and ACP is delivered at lower flow rates (e.g., 10 mL/kg/min) through the axillary artery cannula and thus up the right carotid artery (Fig. 25.9) [22]. This allows bilateral cerebral perfusion, assuming that the circle of Willis is intact. If there is uncertainty about the integrity of collateral blood flow to the left cerebral hemisphere, the left common carotid also can be cannulated directly through the surgical field, as shown. Pressure during this method of ACP can be monitored via a right radial arterial line, but monitoring pressure and maintaining a certain pressure is not known to improve outcome.

Figure 25.9 ACP via right axillary artery cannulation. Figure demonstrates routes of cannulation and monitoring of arterial pressures for extensive arch reconstruction. RA 1, right radial arterial line; RA 2, left radial arterial line. Thick lines indicate native arterial vessels. Thin lines indicate CPB circuit tubing and connectors. Hatched areas indicate Dacron grafts. (From Cook R, Min G, Macnab A, et al. Aortic arch reconstruction: Safety of moderate hypothermia and antegrade cerebral perfusion during systemic circulatory arrest. J Card Surg.2006;21:159, with permission of Blackwell Publishing.)

            Cannulating the right axillary artery instead of the femoral artery to provide CPB before and after circulatory arrest reduces the risk of systemic atheroembolism. This is because right axillary artery cannulation provides antegrade aortic flow, whereas femoral artery cannulation produces retrograde flow through an often atherosclerotic descending aorta [23].

            Additionally, DHCA is required only for completion of the distal and arch anastomoses. Then the aortic graft may be clamped proximally and full CPB perfusion reinitiated to the rest of the body while the proximal anastomosis is performed.

            Many groups accept ACP as the safest method of brain protection during arch surgery [21]. Antegrade perfusion may take advantage of autoregulation of cerebral blood flow, which is thought to remain intact even at low temperatures when α-stat blood gas management is used. With intact autoregulation, physiologic protection against ischemia of hyperperfusion will be active. However, proponents of pH-stat blood gas management argue that the cerebral vasodilation that accompanies elevated pCO2 will produce more uniform cooling and perfusion of the brain (see Chapters 21 and 24).

     5. Complications. Complications from aortic arch surgery include those of any procedure in which CPB is used. Irreversible cerebral ischemia is a distinct possibility with this type of surgery. Hemostatic difficulties may be increased secondary to the multiple suture lines, long CPB times, and prolonged periods of intraoperative hypothermia.

   F. Anesthetic considerations for aortic arch surgery

     1. Monitoring

        a. Arterial BP. An intra-arterial catheter can be placed in either the right or left radial artery, depending on which of the head and neck arteries that extend off of the aortic arch are involved. If both the right- and left-sided arteries are involved, the femoral artery may need to be catheterized. As noted earlier, if the right axillary artery is cannulated for CPB, right radial arterial line BPs will not accurately reflect systemic BP during CPB. If the right axillary artery is used for CPB, and DHCA with ACP is planned, some surgeons may ask that the patient have a right radial arterial line placed for monitoring arterial pressures during ACP. Also, with profound hypothermia, many have found that the radial artery does not provide accurate pressures for a period during rewarming, and they electively and pre-emptively insert a femoral arterial catheter.

        b. Neurologic monitors

           (1) EEG is often used to ensure that the patient has been cooled sufficiently such that the EEG is isoelectric before DHCA. Thiopental or propofol is given by many anesthesiologists to achieve or extend this isoelectric state [24].

           (2) Nasal or oropharyngeal temperature can be used to monitor brain cooling.

           (3) Near-infrared regional spectroscopy (NIRS). This relatively new technology measures frontal cerebral oxygenation through light transmittance. Although the technology is complex, it is easily applied and seems to be most useful as a trend monitor during ascending aortic and arch surgery, particularly when ACP is employed. Significant reductions in left-sided sensor values compared with right-sided ones may indicate an incomplete circle of Willis. We have found that these values are usually restored when separate left carotid perfusion begins. However, clear outcome data are not yet available. Longer periods of lower cerebral oxygenation during DHCA, as indicated by NIRS, have been associated with longer postoperative hospital stays, but large, well-designed prospective studies are needed to validate the efficacy of these approaches [25,26].

        c. TEE. It provides useful information similar to that for ascending aortic surgery (see Section IV.D.1), but care should be taken when placing the probe, because patients undergoing aortic arch surgery are even more prone to developing perioperative coagulopathy.

     2. Choice of anesthetic agents. See Table 25.9.

     3. Management of hypothermic circulatory arrest. The technique involves core cooling to 15 to 20°C, packing the head in ice, using pharmacologic adjuncts to aid in cerebral protection, avoiding glucose-containing solutions, and using appropriate monitoring for selective cerebral perfusion. More details are provided in Chapter 24.

     4. Complications. Complications related directly to anesthesia for aortic arch surgery are uncommon. One potential complication could be myocardial depression secondary to the use of thiopental for cerebral protection; inotropic agents are often needed during weaning from CPB, probably to counter the effects of prolonged myocardial ischemia during DHCA.

   G. Descending thoracic and thoracoabdominal aortic surgery

     1. Surgical approach. Aneurysms of the descending thoracic aorta frequently extend into the abdominal cavity and involve the entire aorta. They are often classified according to Crawford’s classification (Fig. 25.10). Exposure of the affected segment of aorta may be accomplished through a left thoracotomy incision alone or through a thoracoabdominal incision. Extent IV aneurysms involve the supraceliac abdominal aorta but still require thoracic aortic clamping. The patient is placed in a full right lateral decubitus position with the hips rolled slightly to the left to allow access for potential cannulation of the femoral vessels for left heart or CPB. When positioning the patient, it is important to protect pressure points via measures such as using an axillary roll, placing pillows between the knees, and padding the head and elbows. It is also important to maintain the occiput in line with the thoracic spine to prevent traction on the brachial plexus.

Figure 25.10 The Crawford classification of repair for thoracoabdominal aortic aneurysm surgery, with a descending thoracic aortic repair for comparison. The descending aortic repair does not extend beyond the diaphragm, whereas all the others do. Extent I aneurysms involve an area that begins just distal to the left subclavian artery and extends to most or all of the abdominal visceral vessels but not the infrarenal aorta. Extent II aneurysms also begin distal to the left subclavian and involve most of the aorta above the abdominal bifurcation. Extent III lesions begin in the mid-thoracic aorta and involve various lengths of the abdominal aorta. Finally, Extent IV lesions originate above the celiac axis and end below the renal arteries; these aneurysms necessitate a thoracoabdominal approach for proximal aortic cross-clamping.

(Reproduced with permission from Baylor College of Medicine.)

     2. Surgical techniques. Regardless of whether a patient has a descending thoracic aortic aneurysm, a thoracoabdominal aneurysm, a dissection, or aortic rupture, surgical repair usually involves placing aortic cross-clamps both above and below the affected region of the aorta and then opening the aorta and replacing the diseased segment with a graft.

        a. Simple cross-clamping. Some groups report success with cross-clamping the aorta above and below the lesion without using additional measures to provide perfusion distal to the aortic lesion. This technique has the advantage of simplifying the operation and reducing the amount of heparin needed (Fig. 25.11) because more heparin is required when using bypass circuits. However, there is the obvious disadvantage of potentially compromising flow to the distal aorta and its perfused organs when the simple cross-clamp technique is used.

Figure 25.11 Illustration of simple cross-clamp placement for repair of descending aortic aneurysm or dissection. Distal clamp placement dictates that flow to the spinal cord and major organs proceeds through collateral vessels. (From Benumof JL. Intraoperative considerations for special thoracic surgery cases. In: Benumof JL, ed. Anesthesia for Thoracic Surgery. Philadelphia, PA: WB Saunders; 1987:384, with permission.)

            Clamping the descending thoracic aorta generally produces marked hemodynamic changes, with profound hypertension in the proximal aorta and hypotension distal to the cross-clamp. The increase in afterload that occurs when the majority of the cardiac output goes only to the arteries perfusing the head and upper extremities can cause acutely elevated LV filling pressures and a corresponding progressive drop in cardiac output. Presumably, LV failure may result if this increased afterload is maintained for a significant length of time. Furthermore, hypertension in the proximal aorta could precipitate a catastrophic cerebral event, particularly in patients with unidentified cerebral aneurysms. Mean arterial pressure (MAP) distal to the aortic cross-clamp may decrease to less than 10% to 20% of the patient’s baseline BP. This decrease will cause a decrease in renal perfusion and, perhaps, spinal cord perfusion. The physiology of aortic cross-clamping can change depending on the actual site of the clamp and is influenced by many factors, a discussion of which is beyond the scope of this chapter. Gelman’s review of the subject remains an excellent reference [27].

            The presence of chronic obstruction to distal aortic blood flow such as that which occurs with aortic coarctations generally results in well-developed collateral flow and will lessen the hemodynamic changes usually encountered when a cross-clamp is placed on the descending thoracic aorta. This is illustrated by BPs taken proximal and distal to the aortic cross-clamp in a series of patients with aortic coarctations versus descending thoracic aortic aneurysms (Table 25.10) [28].

Table 25.10 Proximal versus distal blood pressure in simple aortic clamping

            Another method of simple aortic cross-clamping is use of an “open” technique, in which no cross-clamp is used distal to the aortic pathology. This technique allows direct inspection of the distal aorta for debris such as thrombus and atheroma, and graft material can be anastomosed in an oblique fashion that reincorporates the maximal number of intercostal arteries.

        b. Shunts. A method that provides decompression of the proximal aorta and perfusion to the distal aorta involves placement of a heparin-bonded (Gott) extracorporeal shunt from the LV, aortic arch, or left subclavian artery to the femoral artery (Fig. 25.12). Systemic heparinization is usually not required. The advantage of this technique is that distal aortic perfusion and proximal aortic decompression are achieved. However, there may be problems related to technical difficulties with placement and kinking of the shunt, which result in inadequate distal flows. Furthermore, only two sizes of these shunts are available: 7 mm (5-mm inner diameter) and 9 mm (6-mm inner diameter). These relatively small diameters may limit blood flow and, thereby, limit the amount of proximal LV decompression and augmentation of distal aortic perfusion that can be accomplished.

Figure 25.12 Placement of a heparin-coated vascular shunt from proximal to distal aorta during repair of descending aneurysm or dissection. (From Benumof JL. Intraoperative considerations for special thoracic surgery cases. In: Benumof JL, ed. Anesthesia for Thoracic Surgery. Philadelphia, PA: WB Saunders; 1987:384, with permission.)

Table 25.12 Management of extracorporeal circulation for surgery of the descending aorta

        c. Extracorporeal circulation (ECC). Historically, the first method used for distal aortic perfusion and proximal decompression in the repair of descending thoracic aortic lesions was ECC. There are several ways to perform ECC, but all involve removal of blood from the patient, passage into an extracorporeal pump, and reinfusion into the femoral artery to provide perfusion distal to the aortic cross-clamp (Fig. 25.13). An alternative technique is to perfuse the body of the aneurysm with ECC while the proximal anastomosis is being performed and then open the aneurysm and perfuse the major visceral vessels individually until they can be incorporated into the anastomosis.

Figure 25.13 Partial bypass (PB) (or extracorporeal circulation [ECC]) method for maintaining distal perfusion pressure and preventing proximal hypertension. Oxygenated blood can be taken directly from the LV or atrium (or aortic arch) and pumped either by roller head or centrifugal pump into the femoral artery. Alternatively, unoxygenated blood can be taken from the femoral vein, passed through a separate oxygenator, and pumped into the femoral artery. Use of an oxygenator dictates the use of a full heparinizing dose. (From Benumof JL. Intraoperative considerations for special thoracic surgery cases. In: Benumof JL, ed. Anesthesia for Thoracic Surgery. Philadelphia, PA: WB Saunders; 1987:384, with permission.)

            Blood can be drained from the patient into the extracorporeal pump from the femoral vein, which is technically the easiest site to access for surgery on the descending thoracic aorta. However, using a venous drainage site necessitates placing an oxygenator in the ECC circuit to provide oxygenated blood for systemic reinfusion. This form of CPB in conjunction with DHCA arrest may be necessary to repair descending thoracic aortic aneurysms that involve the aortic arch.

            Alternatively, LHB may be used. The left atrium, LV apex, or left axillary artery may be cannulated to carry oxygenated patient blood to the ECC pump; this blood is then returned to the distal aorta or femoral artery. This technique does not require an oxygenator in the LHB circuit (Fig. 25.14).

Figure 25.14 Left heart bypass. Perfusing the aneurysm allows completion of the proximal anastomosis while distal perfusion is maintained. After the aneurysm is opened, perfusion of the celiac, superior mesenteric, and renal arteries may be performed by individual cannulation before these arteries are attached to the graft. (From Coselli JS, LeMaire SA. Tips for successful outcomes for descending thoracic and thoracoabdominal aortic aneurysm procedures. Semin Vasc Surg. 2008;21:13–20, with permission.)

            Both of these ECC techniques have disadvantages. Use of an oxygenator requires complete systemic heparinization, which is associated with an increased incidence of hemorrhage, especially into the left lung. Left atrial or ventricular cannulation for LHB without an oxygenator may allow the use of less heparin, but this approach increases the risk for systemic air embolism. Also, in the venous-to-arterial–circulation CPB technique, a heat exchanger is included in the ECC circuit, which helps to avoid significant perioperative hypothermia and corresponding coagulopathy. When LHB is used, a heat exchanger is often not added to the ECC circuit. Table 25.11 summarizes the possible cannulation sites and the major differences between heparinized shunts and ECC for perfusion distal to the aortic cross-clamp.

Table 25.11 Options for increasing distal perfusion in descending aortic surgery

     3. Complications of descending thoracic aortic repairs

        a. Cardiac. Major cardiac morbidity and mortality was approximately 12% in one large series of thoracoabdominal aneurysm repairs [29].

        b. Hemorrhage. Significant perioperative bleeding is a common complication.

        c. Renal failure. The incidence of renal failure in large case series ranges from 13% to 18% [29,30]. The mortality rate is substantially higher in those patients experiencing postoperative renal failure [29]. The cause is presumed to be a decrease in renal blood flow during aortic cross-clamping. However, renal failure may still occur in the presence of apparently adequate perfusion (heparinized shunt or ECC). Pre-existing renal dysfunction increases a patient’s likelihood of developing postoperative renal failure.

        d. Paraplegia. The reported incidence of paraplegia with open surgical repair of aneurysms of the descending thoracic or thoracoabdominal aorta ranges from 0.5% to 38% [2932]. The cause is either complete interruption of blood supply or prolonged hypoperfusion (more than 30 min) [32] of the spinal cord via the anterior spinal artery. The anterior spinal artery is formed by fusion of the vertebral arteries and is the major blood supply to the anterior spinal cord. As the anterior spinal artery traverses the spinal cord from cephalad to caudad, it receives collateral blood supply from radicular branches of the intercostal arteries (Fig. 25.15). In most patients, one radicular arterial branch, known as the great radicular artery (of Adamkiewicz), provides a major portion of the blood supply to the midportion of the spinal cord. It may arise anywhere from T5 to below L1. Unfortunately, this vessel is difficult to identify by angiography or by inspection during surgery. Interruption of flow may lead to paraplegia, depending on the contribution of other collateral arteries to spinal cord perfusion. With anterior spinal artery hypoperfusion, an anterior spinal syndrome can result, in which motor function is usually completely lost (anterior horns) but some sensation may remain intact (posterior columns).

Figure 25.15 Anatomic drawing of the contribution of the radicular arteries to spinal cord blood flow. If the posterior intercostal artery is involved in a dissection or is sacrificed to facilitate repair of aortic pathology, critical blood supply may be lost, causing spinal cord ischemia. (From Cooley DA, ed. Surgical Treatment of Aortic Aneurysms. Philadelphia, PA: WB Saunders; 1986:92, with permission.)

        e. Miscellaneous. Other significant complications may arise during surgery of the descending thoracic aorta. Some of these are specific to the type of aortic pathology being addressed. For example, death from multiorgan trauma and failure is a major entity in patients who initially survive traumatic aortic rupture. Furthermore, thoracic aortic surgical patients are more likely to succumb to respiratory failure or multiorgan failure than patients with isolated abdominal aortic disease. Patients who undergo thoracoabdominal aortic repair may develop postoperative diaphragmatic dysfunction. Cerebrovascular accidents are seen in a small number of thoracic aortic surgical patients. Also, left vocal cord paralysis due to recurrent laryngeal nerve damage commonly occurs during descending thoracic aortic surgery because of the proximity of the nerve to the site of the aneurysm. All descending thoracic and thoracoabdominal aneurysms may be associated with major complications, but Crawford extent II lesions involve more potential hazards because more of the aorta is affected.

   H. Anesthetic considerations in descending thoracic aortic surgery

     1. General considerations. Providing anesthesia for descending thoracic aortic surgery can be extremely demanding because of profound hemodynamic changes and compromised perfusion of organs distal to the aortic cross-clamp. Anesthesia for descending thoracic aortic surgery is summarized in several good reviews [33,34].

     2. Monitoring

        a. Arterial BP. A right radial or brachial arterial catheter is needed to monitor pressures above the proximal clamp because the left subclavian artery may be occluded with the application of the aortic cross-clamp. To assess perfusion distal to the lower aortic cross-clamp, many centers place a femoral artery catheter in addition to the right radial or brachial catheter in order to monitor pressure below the distal clamp. Should the LHB technique of ECC be used, the left femoral artery is typically cannulated for distal perfusion of the aorta, and the right femoral artery can be used for monitoring BP.

        b. Ventricular function. Some operative teams monitor LV function during proximal aortic cross-clamping. A TEE can be useful for directly assessing LV function and volume, but, occasionally, the TEE probe in the esophagus can interfere with the surgical placement of retractors or clamps. In those cases, TEE cannot be used. A PA catheter allows for indirect assessment of LV filling and cardiac output, presuming that the right heart and tricuspid valve function well and the patient does not have pulmonary hypertension. However, a PA catheter is not as helpful as TEE for intraoperative real-time patient monitoring.

        c. Other monitors. ECG lead V5 cannot be used because of the surgical approach, which limits the assessment of anterior myocardial ischemia. However, TEE should allow good assessment of anterior LV wall motion.

     3. One-lung anesthesia. In order to provide good surgical access, double-lumen endobronchial tubes allow deflation of the left lung during surgery on the descending thoracic and thoracoabdominal aorta. This not only improves surgical exposure but also protects the left lung from trauma associated with surgical manipulation. Furthermore, if trauma to the left lung leads to hemorrhage into the airway, the double-lumen tube can protect the right lung from blood spillage. A left-sided double-lumen endotracheal tube may generally be easier for the anesthesiologist to place and is often used for operations on the descending thoracic aorta. However, in some patients, the aortic aneurysm distorts the trachea or left main stem bronchus to the degree that placing a left-sided double-lumen tube is impossible. Patients with aortic rupture may also have a distorted left main stem bronchus. Right-sided double-lumen endobronchial tubes may be used, but proper alignment with the right upper lobe bronchus should be checked with a fiberoptic bronchoscope. Alternatively, use of a single-lumen endotracheal tube with an endobronchial blocker can be considered when a double-lumen tube cannot be placed, or when changing a double-lumen tube over to a single-lumen endotracheal tube is anticipated to be challenging (i.e., the patient has a difficult intubation before undergoing an operation that involves major transfusion and fluid resuscitation). For a detailed description of double-lumen and endobronchial blocker tube placement and single-lung ventilation, see Chapter 26.

     4. Anesthetic management before and during aortic cross-clamping. Before the aorta is cross-clamped, mannitol (0.5 g/kg) is often administered to try to provide some renal protection during aortic cross-clamping, when the kidneys may experience low perfusion. Even when shunting or ECC is used, changes in the distribution of renal blood flow may make efforts at renal protection prudent.


          After the aortic cross-clamp is applied, it is important to closely monitor acid–base status with serial arterial blood gas measurements, as it is common for metabolic acidosis to develop because of hypoperfusion of critical organ beds. Acidosis should be treated aggressively with sodium bicarbonate and with attempts to increase distal aortic perfusion pressure if LHB or shunting is used (particularly if the patient is normothermic). If simple aortic cross-clamping without shunting or ECC is used, proximal hypertension should be controlled, again realizing that distal organ flow may be diminished. In treating proximal hypertension, regional blood flow studies have shown that infusing nitroprusside may decrease renal and spinal cord blood flow in a dose-related fashion. Ideally, aortic cross-clamp time (regardless of technique) should be less than 30 min, because the incidence of complications, especially paraplegia, starts to increase substantially beyond this time [32].

          If a heparinized shunt is used and proximal hypertension cannot be treated without producing subsequent distal hypotension (less than 60 mm Hg), the surgeon should be made aware that there could be a technical problem with the shunt’s placement. If LHB is used, pump speed can be increased such that proximal hypertension can be reduced by moving blood volume from the proximal to the distal aorta. This also simultaneously increases lower-body perfusion. Usually, little or no pharmacologic intervention is needed during LHB, because changing the pump speed allows for rapid control of proximal and distal aortic pressures. Table 25.12 lists the treatment options for several clinical scenarios when using ECC.

          Before the surgeon removes the aortic cross-clamp, the patient should be adequately volume resuscitated, and a vasopressor should be available in case substantial hypotension occurs after the aorta is unclamped. The anesthesiologist must be constantly aware of the stage of the operation so that major events such as clamping and unclamping of the aorta are anticipated.

     5. Declamping shock. When simple cross-clamping of the aorta is used, subsequent unclamping can lead to serious and even life-threatening consequences, usually from severe hypotension or myocardial depression. There are several theoretical causes of declamping syndrome, including washout of acid metabolites, vasodilator substances, sequestration of blood in the gut or lower extremities, and reactive hyperemia. The usual cause, however, is relative or absolute hypovolemia. Anesthesiologists may be fooled into under-resuscitating patients while the aortic cross-clamp is on because of high proximal arterial pressures. To attenuate the effects of clamp removal, the patient’s volume should be optimized, particularly in the 10 to 15 min before unclamping. This includes elevating filling pressures by infusing blood products, colloid, or crystalloids. Some advocate prophylactic bicarbonate administration just before clamp removal to minimize myocardial depression from “washout acidosis.” It is advisable for the surgeon to release the cross-clamp slowly over a period of 1 to 2 min to allow enough time for compensatory hemodynamic changes to occur and for the anesthesiologist to assess whether further volume resuscitation is indicated.

          Vasopressors may be needed to compensate for hypotension after the aortic cross-clamp is removed, but the anesthesiologist should take care not to “overshoot” target BP, as even transient hypertension may result in significant bleeding from the aortic suture lines. With a volume-resuscitated patient and a slow cross-clamp release, any significant post-clamp hypotension is usually short lived and well tolerated. If hypotension is severe, the easiest intervention is reapplication of the clamp and further volume infusion.

          If shunts or ECC are used, declamping hypotension is usually mild, as the vascular bed below the clamp is less “empty,” and there will be less proximal-to-distal aortic volume shifting after the aortic cross-clamp is released. If a volume reservoir is used in the bypass circuit, ECC also provides a means for rapid volume infusion after the aortic cross-clamp is removed.

     6. Fluid therapy and transfusion. Even patients undergoing elective repair of a descending thoracic aneurysm versus aortic rupture or dissection may be relatively hypovolemic. Fluid therapy should have the following aims: correcting the patient’s starting fluid deficit, providing maintenance fluids, compensating for evaporative and “third space” losses, decreasing red cell loss by mild hemodilution, and replacing blood loss as needed.

          Despite proximal and distal control of portions of the aorta undergoing surgical repair, blood loss can be considerable in these cases because of back-bleeding from the intercostal arteries, which are often ligated when the aorta is opened. Use of intraoperative cell-scavenging devices has become common and has reduced the need for banked blood transfusions. However, large-volume blood loss can occur rapidly in these operations, and banked blood transfusions are often needed. As long as liver perfusion is adequate, even with a large blood loss, citrate toxicity is usually not a problem because of rapid “first pass” metabolism in the liver. Repair of a thoracic aneurysm, particularly with simple clamping, however, presents a unique situation because hepatic arterial blood flow to the liver is compromised for an extended period of time. In this circumstance, transfusion of large amounts of banked blood may rapidly produce citrate toxicity, resulting in myocardial depression that requires vigilant calcium chloride infusion.

     7. Spinal cord protection. In addition to the use of ECC, shunts, and expeditious surgery, several other methods have been promoted to protect the spinal cord during aortic cross-clamping [35].

        a. Maintaining perfusion pressure. Some groups prefer to maintain perfusion pressure of the distal aorta in the range of 40 to 60 mm Hg to increase blood flow to the middle and lower spinal cord. This practice should be regarded as controversial because at present, few data exist regarding outcome. No method used to maintain blood flow to the distal aorta (i.e., shunt or partial bypass) guarantees that spinal cord blood flow, and therefore function, will be preserved. Proximal and distal clamp placement to isolate the diseased aortic segment may include critical intercostal vessels that provide blood flow to the spinal cord and whose loss is not compensated for by distal aortic perfusion. In addition, distal perfusion may be hindered by the presence of atherosclerotic disease in the abdominal aorta, a condition that may also compromise blood flow to the kidneys and spinal cord. Finally, these crucial arterial vessels may be disrupted in gaining surgical exposure. The largest studies have shown no difference in the incidence of paraplegia, regardless of the type of surgical adjunct used.

        b. Somatosensory-evoked potentials (SEPs). SEPs have been promoted as a means of assessing the functional status of the spinal cord during periods of possible ischemia [35]. Briefly, SEPs monitor spinal cord function by stimulating a peripheral nerve and monitoring the response in the brainstem and cerebral cortex. Normal SEPs seem to ensure the integrity of the posterior (sensory) columns. However, SEPs have several shortcomings. First, during aortic surgery, the anterior (motor) horns are more at risk. Perhaps for this reason, there have been reports of patients having normal SEPs during cross-clamping but subsequently being found to have paraplegia. Second, it must be remembered that many anesthetics, including all of the halogenated drugs, nitrous oxide, and several IV drugs (e.g., thiopental and propofol), will alter the amplitude and latency of the evoked potential. Ongoing dialogue should therefore occur between the anesthesiologist and the individual(s) performing and evaluating the neuromonitoring during the operation in order to create an anesthetic plan that will be compatible with effective SEP monitoring (i.e., one-half minimum alveolar concentration of volatile anesthetic, etc.). In addition, if simple cross-clamping is used, ischemia of the peripheral nerves will interfere with SEPs interpretation.

            Other than being used as an intraoperative tool to help identify intercostal arteries that should be reimplanted to preserve spinal cord perfusion, SEPs monitoring has not been shown to decrease the incidence of paraplegia.

        c. Motor-evoked potentials (MEPs). Because of the noted deficiencies in SEPs monitoring, the use of MEPs has been advocated as a potentially superior method of monitoring for spinal cord ischemia, because MEP monitoring can accurately assess the integrity of the anterior horn of the spinal cord. However, because access to the central nerve roots for direct stimulation is not possible in thoracic surgery, transcranial stimulation over the motor cortex is used. In addition to being cumbersome, this method has been reported to trigger seizures in susceptible patients. However, some groups have successfully used MEPs, particularly as an adjunct to SEPs, to detect spinal cord injury in patients undergoing thoracic and thoracoabdominal aortic aneurysm repairs. Although studies have shown these neuromonitoring techniques to be helpful for predicting spinal cord injury during operations on the thoracic aorta, these monitoring methods cannot definitively rule out intraoperative spinal cord injury that will result in paraplegia. Therefore, these methods should be used as an addition to, and not a replacement for, intraoperative spinal cord protection strategies such as cerebrospinal fluid (CSF) drainage and other efforts to maintain arterial perfusion of the spinal cord [3638]. As with SEP monitoring, MEP monitoring requires good communication between the anesthesiologist and the neuromonitoring personnel, particularly because neuromuscular blockade cannot be used during intervals where MEP assessments are needed.

        d. Hypothermia. Allowing the core body temperature to passively drift down to 32 to 34°C during surgery will lower the metabolic rate of the spinal cord tissue, possibly providing some protection from reduced or interrupted blood flow. Adequate temperature reduction can be usually accomplished by exposing the patient to a cool operating room. Other methods, such as topical cooling (cooling blankets, bags of crushed ice) and cold saline gastric lavage, also may be used. Precise control of temperature is difficult, though. At temperatures below 32°C, the myocardium may become more prone to ventricular arrhythmias, and there is increased risk of coagulopathy with hypothermia. Despite these potential problems, using vigorous methods to rewarm the patient is ill advised because of the risk of rapidly warming neural tissue that may be ischemic.


        e. CSF drainage. Spinal cord damage may also be mediated by the increases in cerebrospinal fluid pressure (CSFP) that often accompany aortic cross-clamping. CSFP may increase to levels as high as the mean distal aortic pressure. Spinal cord perfusion pressure (SCPP) is proportional to the patient’s MAP minus the CSFP or CVP—whichever is highest. SCPP may be reduced to zero during aortic cross-clamping. One approach to improving perfusion is placement of a lumbar spinal drain, which not only allows for measurement of the CSFP, but also, by removal of CSF, reduces CSFP and increases SCPP, with an apparent reduction in risk of paraplegia [39]. CSF drainage has been shown to significantly decrease postoperative paraplegia and paraparesis in a randomized controlled trial of 145 patients undergoing surgical repair of extent I or II thoracoabdominal aneurysms, with 13% and 2.6% of patients experiencing postoperative paraplegia or paraparesis in the control group versus the spinal drain group, respectively [31].

           (1) Potential complications of spinal drain placement. Removal of CSF in the presence of an elevated intraspinal pressure can provide a gradient for herniation of cerebral structures. Also, CSF drainage, particularly more rapid CSF drainage to lower CSFPs, may cause intracranial bleeding from traction of the brain on the meninges, torn bridging veins, and the formation of subdural hematomas [4042]. Risk of intracranial bleeding may be decreased by maintaining CSFP above at least 10 cm H2O (7.4 mm Hg) during CSF drainage [41]. To reduce the incidence of intracranial hemorrhage and subdural hematoma, some centers have recently changed their practice regarding perioperative CSF drainage in patients with no indications of spinal cord injury (e.g., changes on intraoperative SEP or MEP monitoring, postoperative paraplegia). For these patients, CSF drainage is now targeted to less aggressive minimum CSFP thresholds, such as 10 to 15 mm Hg, and hourly CSF drainage is not to exceed 15 mL/h even if CSFP is above the minimum CSFP. If the patients develop paraplegia, CSF drainage is then liberalized to try to provoke resolution of the paralysis [40]. If a patient develops a subdural hematoma and CSF is still leaking from the insertion site after drain removal, an epidural blood patch may be warranted at the site [41]. In addition, placement of a spinal drain followed by systemic heparinization could lead to the formation of an epidural hematoma at the insertion site [42]. This is of more concern in patients who are undergoing concurrent aortic arch and descending thoracic aortic repairs that involve CPB with full heparinization and DHCA and who are, thus, at increased risk of bleeding. Another risk of drain placement is catheter fracture in the subarachnoid space.

           (2) Technique for inserting and monitoring spinal drains. There are a variety of commercially available spinal drain catheters, but the insertion technique is similar for all. Spinal drain catheters are generally placed using anatomic landmarks through a 14 G (or smaller) Touhy needle that has been inserted into the subarachnoid space at a lumbar interspace (usually L3 to L4 or L4 to L5). Once the catheter is threaded into the subarachnoid space and the needle is removed, the drain is attached to a stopcock that allows toggling between measurement of CSFP and a collection bag for drainage (Fig. 25.16) [43]. Some practitioners remove CSF intermittently to reduce CSFP, while others prefer to allow continuous drainage whenever the CSFP exceeds a predetermined set point. Although many try maintaining CSFP at 8 to 10 mm Hg in order to balance the benefit of increasing SCPP against the risk of supratentorial bleeding with a lower CSFP, there is no consensus in the literature regarding what the optimal target CSFP should be or how much CSF may be removed over a set time period.

Figure 25.16 Intraoperative CSF drainage during thoracoabdominal aortic repair. (From Safi HJ, Miller CC III, Huynh TT, et al. Distal aortic perfusion and cerebrospinal fluid drainage for thoracoabdominal and descending thoracic aortic repair: Ten years of organ protection. Ann Surg. 2003;238:372–380, with permission.)

           (3) Postoperative spinal drain management. There is also no consensus regarding when spinal drains should be removed, and this is of concern considering that 30% or more of all neurologic deficits are delayed in onset [43,44]. Spinal drains are commonly left in for 48 to 72 h postoperatively [31,40] and are replaced if neurologic deficits occur after the drain is removed. In addition to maintaining CSFP between 10 to 15 mm Hg in the postoperative setting, efforts must be made to avoid systemic hypotension and associated decreased spinal cord perfusion. If delayed-onset paraparesis or paraplegia evolves, systemic hypotension should be treated and the CSF drained. This combination of measures can result in some recovery of neurologic function [43]. As with any patient with a dural puncture, headaches related to residual CSF leaks may be expected, and some will require therapy with epidural blood patches. Reviewing our own experience, we recently found that the incidence of post-dural puncture headaches and need for an epidural blood patch were elevated in patients with connective tissue diseases such as Marfan syndrome (Youngblood S, Tolpin D, LeMaire SA, et al., unpublished data; presented at the Annual Meeting of the American Society of Anesthesiologists, Chicago, Illinois, October 2011).

           (4) Other methods of spinal cord protection. Additional “protective” measures, such as IV steroids, pharmacologic suppression of spinal cord function through IV or intrathecal drug administration, local hypothermia, and free radical scavengers, are not widely used or are considered experimental.

     8. Pain relief. Thoracic and thoracoabdominal aortic surgical patients may be given IV opioid and oral analgesics for relief of postoperative pain. However, anesthesiologists may also consider using thoracic epidural anesthesia as an adjunctive perioperative pain-control measure, although, depending upon the length of the surgical incision, analgesic coverage may not be complete. Whereas thoracic epidural analgesia may potentially enhance perioperative pain control, the risk of additional significant complications associated with thoracic epidural placement should also be considered. In a patient who will undergo partial or even full heparinization and who may have significant intraoperative and early postoperative coagulopathy, instrumenting the epidural space may increase the chance of an epidural hematoma (just as placing a spinal drain does). This possibility is particularly worrisome because these patients already have a primary risk of significant neurologic complications. Additionally, it has been reported that use of a thoracic epidural may mask neurologic complications related to the removal of a CSF drainage catheter [45]. Thoracic epidural use may delay the diagnosis and treatment of spinal cord ischemia, such as when a patient cannot move his or her legs postoperatively, and the presence of epidural hematoma or motor blockade related to local anesthesia must also be considered.

     9. Prevention of renal failure. Many patients who require thoracoabdominal aortic repair also present with renal dysfunction. It is therefore important to try to prevent the development of acute or chronic renal failure during the perioperative period. The cause of renal failure is thought to be ischemia from the interruption of blood flow during clamping, although embolism remains another possibility. Use of CPB or a shunt may be protective, but superior outcome data are lacking, and renal failure still occurs despite these surgical adjuncts. Adequate volume loading is probably important for renal protection, and some clinicians also use mannitol. In some centers, cold crystalloid or cold blood renal perfusion is administered during thoracoabdominal aneurysm repair. If the renal arteries can be surgically exposed during periods of the operation when renal arterial blood flow is interrupted, perfusate can be administered with a roller-head pump into perfusion catheters that are inserted into the renal arteries [46]. In a randomized controlled trial, intermittent cold crystalloid renal perfusion prevented postoperative renal dysfunction more effectively than renal perfusion with isothermic blood [47]. Another randomized, controlled trial indicated that cold crystalloid and cold blood renal perfusion produced comparable renal outcomes [48].

   I. Endovascular (EV) graft repair of the thoracic aorta. Successful EV graft abdominal aortic aneurysm repair was first reported in 1991 [49]. Since then, EV graft design has improved to allow reliable deployment in the higher pulse pressure zones of the thoracic aorta, permitting repair of thoracic aortic aneurysms and dissections that were previously only reparable with open procedures. Initially, EV grafting of the descending thoracic aorta was only possible in relatively straight sections of the aorta with good “landing zones” for the proximal and distal portions of the EV graft and no major branches of the aorta in that region. Surgeons are now performing carotid-to-subclavian or aorta-to-visceral bypass operations before EV graft placement to permit placement of these devices where they would otherwise occlude the origin of a critical vessel. This has led to EV therapy of more complex aortic arch and descending thoracic aortic lesions.

     1. Surgical approach. Placing EV grafts in the thoracic aorta generally requires femoral arterial access through which fluoroscopically guided wires and catheters may be passed to allow optimal EV graft positioning. The femoral artery is exposed and isolated via a small groin incision, but, if the femoral artery is too small or stenotic to accommodate the relatively large thoracic EV graft delivery system, a retroperitoneal dissection may be required to attain access to the iliac artery. There have been reports of EV grafts placed into the descending thoracic aorta via alternative arterial access sites such as the axillary arteries, but the femoral artery remains the typical access site for EV graft delivery [50]. The delivery system is positioned fluoroscopically at the desired implantation site, and when the delivery device is withdrawn, the endograft expands at this final aortic position. After EV graft deployment, fluoroscopy and TEE are generally used to reassess for blood leakage around the graft [51]. Patients are positioned supine on the fluoroscopy table throughout the procedure.

     2. Surgical techniques

        a. Patients must be systemically anticoagulated, usually with heparin, during the proce-dure.

        b. It is important that patients do not move during angiography, particularly during EV graft deployment. Sometimes the interventionalist will ask the anesthesiologist to hold respirations during the procedure so that they may more closely assess the portion of the aorta in which the EV graft will be deployed. This is one reason why EV graft placement into the descending thoracic aorta is usually performed with general anesthesia.

        c. EV grafts are designed to withstand continuous forward and pulsatile forces of blood flow in the aorta. Advances have led to the development of self-expanding stents that reliably adhere to the aortic wall after deployment and do not require temporarily occlusive balloon inflation within the aorta. This removes the risks of proximal hypertension associated with aortic occlusion within the thoracic aorta.

        d. EV graft design is evolving rapidly, and therefore, the number of patients ineligible for EV grafts is decreasing. However, there remain limitations regarding who can receive an EV graft in the descending thoracic aorta. The patient’s aortic pathology must have a proximal “landing zone” of at least 10 to 15 mm in length and a diameter not greater than the diameter of the largest available EV graft [52]. Many descending thoracic aneurysms and dissections involve the distal aortic arch, including the takeoff of the left subclavian artery. EV stent grafts are now placed that cover the ostia of the left subclavian artery, but prophylactic preprocedural left subclavian artery transposition or left subclavian-to-left common carotid artery bypass is frequently performed for the purpose of trying to prevent post-EV graft complications, including left arm ischemia, stroke, and spinal cord ischemia [53,54]. These complications can occur because the left subclavian artery not only is the main source of blood flow to the left arm, but branches into the vertebral artery (which contributes to the blood flow to the posterior portion of the Circle of Willis), the left internal mammary artery, and costocervical trunk [54]. Myocardial ischemia in patients who have a patent left internal mammary arterial bypass graft is also possible when the left subclavian arterial takeoff is covered by an EV graft [54]. It is important to note that stroke can also occur as a complication of left subclavian artery transposition or left subclavian-to-left common carotid artery bypass, so patients’ cerebral blood flow anatomy and institutional comfort with performance should be considered before left subclavian arterial revascularization is performed [54]. The distal site for EV graft attachment needs to be nonaneurysmal and also of sufficient length. Furthermore, fenestrated stents are being developed to accommodate aortic side branches, but the location of aortic side branches still must be carefully evaluated and considered when one is selecting and placing EV grafts. Aortic tortuosity, calcification, and atheromatous disease are also considerations in determining whether a patient is an appropriate candidate for EV graft placement.

     3. Advantages of EV graft repair

        a. Reduced mortality. Randomized controlled trials have shown significantly decreased mortality in patients undergoing EV repair of abdominal aortic aneurysms [55,56]. Nonrandomized studies of descending thoracic aorta repair have associated EV grafting with significantly lower 30-day mortality than open surgical repair; however, this mortality benefit may not persist at 1 yr after thoracic aortic repair [57]. The randomized controlled INvestigation of STEnt-grafts in Aortic Dissection (INSTEAD) trial reported no significant 2-yr mortality advantage for EV stenting versus medical therapy alone in patients with uncomplicated Type B dissections [58].

        b. Reduced morbidity. Patients experience substantially less blood loss with EV procedures and are spared the prolonged recovery and pulmonary complications that often occur with large thoracoabdominal incisions. EV procedures also allow for increased hemodynamic stability and decreased ischemic risk to the heart and other organs when compared with open repairs. Patients with pulmonary and cardiac comorbidities that would eliminate them as candidates for open repair are often acceptable candidates for thoracic aortic EV graft placement. A recent meta-analysis of 42 nonrandomized studies that included 5,888 patients with aneurysm, trauma, or dissection of the descending thoracic aorta revealed that patients who underwent EV repair versus open surgical repair had significantly less perioperative paraplegia, cardiac complications, transfusions, reoperation for bleeding, renal dysfunction, and pneumonia, and they had a shorter hospital length of stay [57]. In addition, many patients who undergo EV repair require substantially shorter intensive care unit (ICU) stays [52,59,60].

     4. Complications of EV repair

        a. Need for emergency conversion to open repair may occur if the aorta is ruptured or dissected during manipulations to place the EV graft or if the EV graft becomes malpositioned such that it presents substantial risk for visceral ischemia.

        b. Bleeding. Although blood loss during EV repair of the thoracic aorta is markedly lower (approximately 500 mL) [59] than blood loss with open surgery, bleeding does occur from the femoral artery introducer when it is traversed by wires and catheters during the interventional procedure. Because many patients with thoracic aortic disease have comorbidities that make anemia unfavorable, bleeding may be significant enough to warrant periprocedural blood transfusion. Large-volume blood loss may also occur if the internal iliac artery is damaged during removal of what is generally a large-diameter graft deployment device. Massive blood loss should be anticipated in the setting of aortic rupture.

        c. Endoleak. Endoleak occurs when blood continues to flow into the aneurysmal sac after EV graft placement. It confers continued risk of aortic rupture and thus requires early identification and intervention. If identified, responses range from observation over several months to see if the leak resolves spontaneously to another EV procedure to occlude the source of the leak to, in some cases, an open surgical repair. The degree of intervention depends upon the type of leak identified [52]. Type I endoleaks occur with an inadequate seal between the EV graft and the wall of the aorta at either the proximal or the distal attachment site, such that there is persistent flow into the native aneurysm. A Type II endoleak occurs when the portion of the aorta that was to be excluded by the graft fills in a retrograde fashion from back-bleeding collateral vessels, such as the lumbar or inferior mesenteric arteries. There is no definitive approach for addressing Type II endoleak: Both observation and side-branch embolization are used. A Type III endoleak occurs from failure within the EV graft itself and requires conversion to an open repair so that the EV graft does not dislodge.

        d. Stroke. The incidence of periprocedural stroke is ~5% [57] and appears to be higher in patients who undergo EV graft placement in the region of the distal arch that includes the take-off of the left subclavian artery. Among patients who undergo EV graft placement across the left subclavian artery, stroke risk may be lower in those who undergo a staged carotid-to-subclavian-artery bypass procedure first, as this may prevent vertebrobasilar arterial insufficiency and potential ensuing posterior cerebral infarction [54]. Stroke risk is increased in patients with a history of stroke, patients whose CT scans reveal severe atheromatous disease of the aortic arch, and patients in whom EV grafting involves the distal aortic arch [61]. For these reasons, it seems likely that stroke is secondary to embolic events that result from intra-aortic or carotid arterial manipulation during positioning and deployment of the EV graft.

        e. Paraplegia. Although some data suggest that the risk of lower-extremity paraparesis or paralysis is reduced in patients undergoing EV graft versus open thoracic aortic repair, its incidence is still 3% to 4% [57,59,62]. Many surgeons and interventional radiologists, therefore, prefer that a lumbar spinal drain be placed before the procedure and that CSF drainage be conducted in the same manner as described in this chapter for open thoracoabdominal operations.

        f. Contrast nephropathy (CN). Although patients undergoing open aortic surgical repairs are susceptible to postoperative acute renal failure from ischemia during aortic cross-clamping, patients undergoing EV graft repairs are susceptible to CN. Patients with pre-existing renal insufficiency, especially those with diabetic nephropathy, are particularly susceptible to CN [63]. Older age, hypertension, repeat contrast exposure within a short time, use of high osmolality contrast, and preprocedural medications such as nonsteroidal anti-inflammatory drugs and ACE inhibitors also put patients at increased risk for CN [63]. Although the pathogenesis of CN is not completely understood, it appears to be related to decreased renal medullary perfusion and associated ischemia, as well as a direct toxic effect of contrast on the renal epithelial cells. We refer the reader to two excellent reviews of CN for a more detailed discussion [63,64].

   J. Anesthetic considerations for patients undergoing EV stent graft repair of the thoracic aorta

     1. General considerations

        a. Although thoracic aortic EV graft placement is a minimally invasive procedure, the possibility of aortic rupture, dissection, or malposition of the EV graft should be considered when the location for the procedure is selected and the anesthetic planned, as any of these complications would require urgent or emergent conversion to an open procedure. If the procedure cannot be conducted in an operating room because it lacks appropriate angiographic equipment, the entire care team involved with the procedure in a radiology suite must be familiar with resuscitation plans and with transport plans to the operating room. If a cardiac or vascular surgeon is not performing the EV graft procedure, he or she should be immediately available if conversion to open surgery is necessary.

        b. Although there have been reports of placing thoracic aortic EV grafts under regional anesthesia, this approach has several disadvantages in comparison to general anesthesia.

           (1) In the event that there needs to be an emergency conversion to open aortic repair, this conversion will be slowed by the need for airway control before positioning the patient for the operation.

           (2) If the patient is intubated at the start of the procedure and the surgeon feels that the patient is at reasonably high risk for open conversion, the anesthesiologist can place a bronchial blocker in the left main stem bronchus without inflating it. The bronchial blocker can then be quickly inflated in the setting of emergency conversion to provide single-lung ventilation.

           (3) Many of the thoracic aortic EV graft procedures are too lengthy for regional anesthesia.

           (4) General anesthesia with endotracheal intubation allows the anesthesiologist or cardiologist to conduct TEE evaluation throughout the procedure. This has been found to be particularly useful in assessing for endoleaks and for differentiating slow blood flow associated with the porosity of the EV stent graft from true high-velocity peri-stent endoleaks [51,52,65]. In patients undergoing EV stent graft placement for complicated Type B dissections, TEE can also be helpful for repositioning the guidewire from the false to the true lumen and for detecting new intimal tears in the thoracic aorta after EV stent placement [65]. Such new distal aortic tears might require additional EV stents to be placed.

     2. Monitoring. All patients should have standard ASA monitors and a radial arterial line for BP monitoring to help in maintaining hemodynamic stability. The majority of patients presenting for thoracic aortic EV grafts have significant cardiovascular comorbidities that warrant tight hemodynamic control. Furthermore, surgeons may request transient, mild hypotension during stent deployment to help prevent graft migration. In the event that emergent conversion to open surgery is needed, an arterial line will be extremely useful in guiding volume resuscitation and possible cardiopulmonary resuscitation. The location of arterial access for stent delivery should be discussed with the surgical team, because, if the femoroiliac vasculature is not adequate for the procedure, they may guide stent placement via a brachial artery. Typically, a right radial arterial line is ideal for hemodynamic monitoring because it allows monitoring of arterial pressure proximal to the distal aortic arch. Central venous access for monitoring right atrial pressure and for effective administration of vasoactive drugs is reasonable for most patients. Some centers monitor SEPs and/or MEPs, as well as CSFP, during placement of thoracic aortic EV grafts. Urine output should be monitored to help assess adequacy of fluid administration during what can often be long procedures. A fluid warmer and warming blanket should be used if possible to help prevent hypothermia, and oropharyngeal temperature should be monitored.

     3. Fluid therapy and transfusion

        a. Large-bore IV access should be placed in case of the need for rapid volume resuscitation.

        b. Cross-matched, packed red blood cells should be available.

        c. A system for rapid infusion of blood products and other fluids should be immediately available in cases where volume resuscitation is needed.

     4. CSF drainage. Risk for paraplegia or paraparesis after EV graft placement remains approximately 3% to 4%, as noted above, particularly if long segments of the descending thoracic aorta are involved in EV graft placement or if the patient has previously undergone abdominal aortic aneurysm repair [52,66,67]. Therefore, many surgeons, interventionalists, and anesthesiologists prefer to place and manage lumbar spinal drains for EV graft procedures in the manner described above. IV hydration and vasopressor drugs should be administered to maintain higher MAPs. As with patients who undergo open surgical repairs of the descending thoracic aorta, delayed-onset paraparesis or paraplegia also occurs in patients who receive EV stent grafts [66,67], so patients should undergo frequent post-procedural neurologic examinations, and if signs of spinal cord ischemia/injury are detected, aggressive efforts should be made to increase MAPs and to drain more CSF.

     5. CN. Because EV grafting of the thoracic aorta is often a long procedure that involves a substantial volume of IV contrast, the anesthesiologist should consider strategies to attenuate risk for CN, particularly in patients presenting with renal insufficiency.

        a. Hydration. Studies suggest that preprocedural hydration with 0.9% normal saline is beneficial in mitigating the risk of developing CN [63]. There is no consensus regarding the duration of IV 0.9% normal saline infusion before or after the procedure, but avoiding hypovolemia in these patients during the procedure is advisable [64].

        b. N-acetylcysteine (NAC). NAC has antioxidant and vasodilatory effects. Some studies have shown a benefit in pretreating patients with NAC for 24 h before procedures requiring IV contrast, while other studies have shown that there is no benefit [63,64].

        c. Diuretics. Diuretic use does not seem to prevent CN. Some advocate that, if possible, diuretics be withdrawn for the 24 h before procedures requiring contrast [63] because of concern that they may increase the risk of CN.

        d. Dopamine and fenoldopam. Neither of these drugs has been found to prevent CN in human studies [63].

   K. Future trends. Just as the past several decades of treatment of aortic diseases have been marked by innovation and the refinement of surgical and anesthetic techniques, so also will future years. The most promising recent developments have been made in the area of EV stenting of aneurysmal, dissected, or traumatically transected segments of the thoracoabdominal aorta. EV stent graft technology will probably continue to advance, with the industry focusing on newer fenestrated grafts that will not obstruct blood flow to important aortic side branches and other grafts that are able to adhere to curved portions of the aorta, such as the aortic arch. There will also probably be innovations regarding alternate arterial access points for inserting EV stent-deployment devices. Hopefully, greater strides will also be made toward even better protection strategies for organs (i.e., spinal cord, gut, and kidneys), including novel approaches to mitigating end-organ ischemia-reperfusion injury. Anesthetic developments will focus on refining understanding of the physiology of organ preservation and the pharmacology needed to achieve this. Such advances should continue to improve the survival of patients with thoracic aortic disease.


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