Ascending Aorta Repair Case Study

CHAPTER 24. Anesthetic Management for Thoracic Aneurysms and Dissections

Thomas M. Skeehan and John R. Cooper, Jr.

In the management of thoracic aortic surgery, the anesthesiologist may face a marked variability in the problems associated with etiology, type, and anatomic location of the surgical procedure. This chapter gives a concise overview of the pathophysiology of thoracic aortic surgery, an understanding of its surgical approaches and results, and a rational approach to the management of the patient undergoing thoracic aortic surgery.

  1. Classification and natural history

    1. Dissections. An aortic dissection occurs when blood penetrates the aortic intima and forms an expanding hematoma within the vessel wall, usually separating the intima and media to create a so-called false lumen or dissecting hematoma. The vessel lumen is not dilated and often is compressed by the advancing hematoma. In contrast, an aortic aneurysm involves dilation of all three layers of the vessel wall and has a highly different pathophysiology and implications for management. The term dissecting aneurysm, although commonly used, is often a misnomer.

      1. Incidence and pathophysiology

        1. Incidence. Aortic dissections have been estimated to cause one of every 10,000 hospital admissions. In large autopsy series, aortic dissection has been found in one of every 600 cases, and it was believed that dissections may have caused or contributed significantly to the mortality in up to 1% of these autopsy cases.

        2. Predisposing conditions. The medical conditions predisposing to aortic dissection are listed in Table 24.1 in their order of importance. Interestingly, atherosclerosis by itself may not contribute to the risk of subsequent dissection.

        3. 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 also may occur during cannulation for cardiopulmonary bypass (CPB).

        4. 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 24.2. 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.

          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.

        5. 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.

        6. 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 reenters the true lumen. The presence or absence of an exit point does not appear to have an impact on the clinical course.

        7. 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 the occlusion of their lumens by mechanical compression by the false lumen or 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 24.3.

      2. DeBakey classification of dissections (Fig. 24.1). This classification comprises three different types, depending on where the intimal tear is located and which section of the aorta is involved.

        FIG. 24.1 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, et al. Surgical management of dissecting aneurysms of the aorta. J Thorac Cardiovasc Surg 1965;49:131, with permission.)

        1. 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.

        2. 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.

        3. Type III. The intimal tear is located in the descending segment, and the dissection almost always involves the descending portion of the thoracic aorta only, starting just distal to the origin of the left subclavian artery. By definition, type III dissections can propagate proximally into the arch, but this is rare.

      3. Stanford (Daily) classification of dissections (Fig. 24.2). This classification is simpler than the DeBakey classification and has more clinical relevance.

        FIG. 24.2 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, et al. Aortic dissections. J Thorac Cardiovasc Surg 1979;78:367, with permission.)

        1. 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.

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

      4. Natural history

        1. Mortality—untreated. The survival rate of untreated patients with aortic dissections is dismal, with a 2-day mortality of up to 50% in some series and a 6-month mortality approaching 90%. The usual cause of death is rupture of the false lumen and fatal hemorrhage. Other causes of death include progressive cardiac failure (aortic valve involvement), myocardial infarction, stroke, irreversible coma, and bowel gangrene (mesenteric artery occlusion).

        2. Surgical mortality. The overall surgical mortality is approximately 30%, but surgical therapy is often the only viable option for most of these patients.

    2. Aneurysms

      1. Incidence. Thoracic aortic aneurysms account for 1% to 4% of aneurysms seen at autopsy. Currently, approximately 60% involve the ascending aorta and 30% are localized to the descending aorta. Aneurysms involving the aortic arch exclusively make up less than 10% of the total.

      2. Classification by location and etiology. In general, the etiology and pathophysiology of aortic aneurysms are site dependent. The most common causes by region are medionecrosis in the ascending aorta and atherosclerosis in the arch and descending aorta. Other etiologies are listed in Table 24.4.

      3. Classification by shape

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

        2. Saccular. Saccular aneurysms involve only one portion of the aortic wall. Aortic arch aneurysms are commonly of this type.

      4. Natural history. The usual history of aortic aneurysms is that of progressive dilation and, in more than 50% of cases, rupture. The untreated 5-year survival is approximately 13%, depending on the size of the aneurysm at diagnosis. Other complications 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 cerebral vascular accident.

    3. Thoracic aortic rupture (tear)

      1. Etiology. The overwhelming majority of thoracic ruptures are secondary to trauma and almost always involve a deceleration injury in a motor vehicle accident. Sudden deceleration places large mechanical stresses on the aortic wall at points where the aorta is relatively immobile. Rupture of the aorta in many cases leads to immediate exsanguination and death. However, in approximately 10% to 15% of cases, the integrity of the lumen is maintained by the adventitial covering of the aorta, and these patients are able to reach emergency care. Surgical treatment of these survivors is often successful.

      2. Location. The location of most ruptures of the thoracic aorta is the area just distal to the origin of the left subclavian artery (isthmus), due to the relative fixation of the aorta at this point by the ligamentum arteriosum (Fig. 24.3). The aorta also is fixed in the ascending portion just distal to the aortic valve, and this is the second most common site of rupture.

        FIG. 24.3 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: WB Saunders, 1986:186, with permission.)

  2. Diagnosis

    1. Clinical signs and symptoms (Table 24.5)

      1. Dissections. The clinical presentation of aortic dissection usually is characterized by a dramatic onset and a fulminant course. Differences and clinical presentation of Stanford types A and B are listed in Table 24.5.

      2. Aneurysms. Aneurysms of the ascending, arch, or descending thoracic aorta often are 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. In this setting, signs and symptoms are similar to those seen with aneurysms of the descending thoracic aorta if the patient survives the initial event.

    2. Laboratory diagnosis

      1. Electrocardiogram. A common finding for many patients with aortic disease is that of left ventricular hypertrophy, a condition correlating with a history of accompanying hypertension. The electrocardiogram (ECG) may show a pattern associated with ischemia or pericarditis caused by coronary artery occlusion or hemopericardium, respectively, in the setting of ascending aortic dissection.

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

      3. Serum chemistries. There are no specific laboratory findings with asymptomatic aneurysm. Dissection or rupture will produce a fall in hemoglobin. Dissections may cause elevation of cardiac enzymes (coronary artery occlusion), elevation of blood urea nitrogen and creatine (renal artery occlusion), and acidosis (low cardiac output or bowel ischemia).

      4. Computed tomographic scans and magnetic resonance imaging. Computed tomography is a useful tool for diagnosing aneurysm size and has replaced angiography in some instances. Magnetic resonance imaging has been found to be extremely sensitive and specific in terms of identifying the entry tear, false lumen, aortic regurgitation, and pericardial effusion associated with aortic dissections [1].

      5. Angiography. This technique remains the "gold standard" for determining the severity and extent of aneurysm and dissection. It can be used to determine the site of an intimal tear in the setting of dissecting hematoma, to assess aortic valve function, and to identify the distal and proximal spread of the lesion. In the case of ascending aortic pathology that will require CPB, the coronary anatomy can be delineated. Patients with disease of the thoracic aorta usually have concurrent coronary disease. Bypassing significant lesions would help to improve ventricular function for weaning from CPB. Aortography can diagnose the involvement of major vessels but rarely can identify the critical intercostal vessels that provide blood supply to the spinal cord (see Section IV.G).

      6. Transesophageal echocardiography. Transesophageal echocardiography (TEE) has a role in diagnosing and screening patients who are suspected of having an aortic dissection. It can be diagnostic if adequate images are obtained. Pulsed Doppler and color Doppler imaging will aid in diagnosing the presence, extent, and type of dissection in most cases. TEE has been found to be highly sensitive and specific in the diagnosis of aortic dissection. Identification of a mobile intimal flap provides a prompt bedside diagnosis that can be lifesaving. In addition, (a) entry and reentry tears can be defined; (b) aortic regurgitation can be identified and quantified; (c) assessment of left ventricular (LV) function can be made; (d) presence of pericardial effusion or cardiac tamponade can be identified; and (e) follow-up studies of the false lumen can be made after therapeutic intervention.

      7. Recommendation for diagnostic strategies. Nienaber et al. [2] and colleagues proposed a noninvasive imaging strategy for the diagnosis of thoracic aortic dissection. Magnetic resonance imaging, because of its high degree of sensitivity (98.3%) and specificity (97.8%), was recommended as the preferred diagnostic method in hemodynamically stable patients. For patients deemed unstable for this rather lengthy procedure (40 to 45 minutes), TEE, which has an average duration of about 15 minutes and sensitivity and specificity of 97.7% and 76.9%, respectively, is recommended for the unstable patient. Aortography, because of its inability to provide more critical information than the noninvasive methods and its higher incidence of complications, should remain as a diagnostic tool to be used only in select cases.

    3. Indications for surgical correction

      1. Ascending aorta

        1. Dissections. Currently, any acute type A dissection should be corrected surgically, given the virulent course and high mortality if left untreated.

        2. Aneurysms. Surgical indications for resection include the following:

          1. Presence of persistent pain despite a small aneurysm

          2. Involvement of the aortic valve producing aortic insufficiency

          3. Presence of angina due either to LV strain from aortic valve involvement or coronary artery involvement by the aneurysm

          4. Rapidly expanding aneurysm or an aneurysm greater than 10 cm in diameter, because the chance of rupture increases with increasing size

      2. Aortic arch

        1. Dissections. Acute dissection limited to the aortic arch is an indication for surgery (rare).

        2. Aneurysms. Because even elective surgical treatment for these types of aneurysms is more difficult and is associated with a higher morbidity and mortality, management tends to be more conservative. Surgical indications include the following:

          1. Persistence of symptoms

          2. Aneurysm greater than 10 cm in transverse diameter

          3. Progressive expansion of an aneurysm

      3. Descending aorta

        1. Dissection. Some controversy remains concerning the best treatment for an acute type B dissection. Due to similar mortality statistics for medical or surgical intervention, type B dissections often are treated medically in the acute phase, especially if the patient's concurrent disease would make surgical mortality prohibitively high. However, in patients with a type B dissection, the following complications should be treated surgically as they occur:

          1. Failure to control hypertension medically

          2. Continued pain (indicating progression of the dissection)

          3. Enlargement on chest x-ray film, computed tomographic scan, or angiogram

          4. Development of a neurologic deficit

          5. Evidence of renal or gastrointestinal ischemia

          6. Development of aortic insufficiency

            It should also be noted, as shown in Table 24.6, that 10-year survival for patients with medically managed type B dissections is similar to surgical survival for type A and B dissections together. Both of these managements compare favorably with the 10-year survival of patients with untreated aortic dissections.

        2. Aneurysm. Surgical indications include the following:

          1. Chronic aneurysm of the descending thoracic aorta that causes persistent pain or other symptoms

          2. Aneurysm greater than 10 cm in diameter

          3. Expanding aneurysm

          4. Leaking aneurysm (more fulminant symptoms)

  3. Preoperative management of patients requiring surgery of the thoracic aorta. Emergency preoperative management of aortic dissections is discussed below. However, emergency preoperative management for a leaking thoracic aneurysm and a contained thoracic rupture would be similar.

    1. Prioritizing: making the diagnosis versus controlling blood pressure. In the setting of a suspected dissecting hematoma, aortic tear, or leaking aneurysm, the first priority must always be to control the blood pressure (BP). Making the diagnosis with chest x-ray film or angiogram should occur only when proper monitoring, intravenous (IV) access, and therapy have been established. During the diagnostic procedure, the patient should be monitored closely, with a physician present as the clinical situation dictates. The anesthesiologist should become involved as early as possible to lend expertise in monitoring and in airway and hemodynamic management, should clinical deterioration occur before the patient reaches the operating room. Rapid diagnosis using TEE may save critical minutes in initiating definitive surgical treatment in this setting.

    2. BP control. The ideal drug to control BP would be a rapid acting, IV administered drug that has an ultra-short half-life and few if any side effects. Not only systolic and diastolic pressures but also the ejection velocity must be reduced because both of these factors have been shown to be important in the propagation of dissecting hematomas.

      1. Monitoring. It is imperative that these patients have the following: an ECG for detection of ischemia and dysrhythmias; two large-bore IV catheters; an arterial catheter in the proper location (to be discussed); and, if time permits, a central venous catheter or pulmonary artery (PA) catheter to follow filling pressures and to allow drug infusion.

      2. Agents

        1. Vasodilators

          1. Nitroprusside has emerged as the agent of choice for controlling the BP, because it is effective and easily regulated because of its short duration of action. It is given as an IV infusion, and central administration is optimal. 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 toxicity (see Chapter 2).

          2. Nitoglycerin causes direct vasodilation, but it is less potent than nitroprusside. It can be useful in the setting of myocardial ischemia with ascending aortic pathology. Dosages usually range from 1 to 4 μg/kg/min.

          3. Fenoldopam is a newer rapid-acting vasodilator that is a D1-like dopamine receptor agonist. It has little affinity for the D2-like, α1, 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 sparing effects while treating acute hypertension. Dosing starts at 0.05 to 0.1 μg/kg/min and can be incrementally increased to a maximum of 0.8 μg/kg/min.

        2. Decreasing ejection velocity. Decreasing ejection velocity becomes an important therapeutic consideration, especially if nitroprusside is used as the agent to lower BP. Nitroprusside will increase ejection velocity by increasing dP/dt and heart rate. For this reason, β-adrenergic blockade should be used with nitroprusside not only to decrease tachycardia but also to decrease contractility (see Chapter 2).

          1. Propranolol can be administered as an IV bolus of 1 mg, and doses of up to 4 to 8 mg may be required until the effect is seen.

          2. Labetalol, a combined α- and β-blocker, may offer a single alternative to the nitroprusside–propranolol combination. It should be given initially as a 20-mg loading bolus, and several minutes should be allowed for its effect to be seen. If no effect is seen, the dose should be doubled and several minutes allowed again for onset of effect. This process should be repeated up to a maximum dose of 40 to 80 mg every 10 minutes until a total dose of 300 mg is reached or until BP is controlled. Continuous infusion starting at 1 mg/min may be used, or a small bolus dose can be repeated every 10 to 30 minutes to maintain BP control.

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

      3. Desired endpoints. BP should be lowered to approximately 105 to 115 mm Hg systolic, and heart rate should be kept at 60 to 80 beats/min. If a PA catheter is in place, the cardiac index may be lowered to the 2 to 2.5 L/(min·m2) range because a hyperdynamic myocardium may promote the progression of a dissecting hematoma.

    3. Transfusion. A total of 8 to 10 units of blood should be typed and cross-matched before surgery. Use of blood scavenging devices has decreased the amount of banked blood used, but the logistics of processing scavenged blood, plus the clinical situation, may require that homologous transfusion still be used.

    4. Assessment of other organ systems

      1. Neurologic. The patient should be monitored closely to detect signs of any change in neurologic status, because deterioration in function is an indication for immediate surgical intervention.

      2. Kidneys. Renal function should be followed closely with insertion of a urinary catheter. If aortic dissection has been diagnosed, the development of anuria or oliguria in the setting of euvolemia is an indication for immediate surgical intervention.

      3. Gastrointestinal. Serial abdominal examinations should be performed. In addition, blood gas analysis should be done routinely to assess changes in acid–base status, because ischemic bowel can produce significant acidosis.

    5. Use of pain medications. Patients with aortic dissections may be anxious and in severe pain. Pain relief should be given not only to lessen suffering but also to aid in control of BP. It is important to avoid obtundation; otherwise, important changes in patient status will be missed. Worsening of back or abdominal pain may indicate expansion of the lesion or further dissection and is regarded by many surgeons as an emergent situation. In addition, propagation of a dissection into a head vessel may lead to a change in mental status that may be undetected if the patient is oversedated.

  4. Surgical and anesthetic considerations

    1. Goal of surgical therapy (for dissections, aneurysms, aortic rupture). The first major goal of treating acute aortic disruption must be to control hemorrhage. Once control is achieved, the objectives of management of both acute and chronic lesions are similar: to repair the diseased aorta and to restore relationships of major arterial branches.

      Elective repair of a thoracic aneurysm most often is accomplished by replacing the diseased segment of aorta with a synthetic graft and then implanting major arterial branches into the graft. With a dissection, in contrast, the major goal is to resect the segment of aorta containing the intimal tear. When this segment is removed, it is possible to obliterate the false lumen and interpose graft material. It may not be possible or necessary to replace all of the dissected portion of the aorta because, if the origin of dissection is controlled, reexpansion of the true lumen may compress and obliterate the false lumen. With contained aortic tears, the objective is to resect the area of the tear and either reanastomose the natural aorta to itself in an end-to-end fashion or use graft material for the anastomosis if there is insufficient natural aorta remaining.

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

      1. Key principles

        1. Managing BP. BP control must be maintained 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.

        2. Monitoring of organ ischemia. The organs that must be monitored continuously for adequacy of perfusion are the central nervous system, heart, kidney, and lungs. The liver and gut cannot be monitored continuously, but their metabolic functions can be checked periodically.

        3. Treating coexisting disease. Patients with aortic pathology often have associated cardiovascular and systemic diseases, as outlined in Table 24.7.

        4. Controlling bleeding. Achieving hemostasis after CPB or with graft material in place poses special challenges, especially when the native tissue is damaged or diseased. Coagulation abnormalities and their treatment are discussed in Chapter 18.

      2. Induction and anesthetic agents. Because many of these patients come to surgery emergently, most are considered to have a full stomach and require rapid securing of the airway. On the other hand, these patients also require a smooth induction, because wide swings in hemodynamics may worsen the clinical situation. Usually a compromise is made using a controlled induction with cricoid pressure and manual ventilation. This "modified" rapid sequence induction allows some airway protection and expeditious titration of anesthetic drugs to control BP, the main goal being to secure the airway as quickly as possible with a minimum of hemodynamic perturbation. Use of nonparticulate antacids, H2-blockers, and metoclopramide should be considered before induction of anesthesia. Anesthetic considerations and agents are described more fully in Section IV.D. Despite all precautions, marked changes in hemodynamics are common and should be expected [3].

      3. Importance of site of lesion (Table 24.8). Although the principles of anesthetic induction and choice of anesthetic agents are similar for all aortic lesions, practical intraoperative management depends almost entirely on the site of the lesion.

    3. Ascending aortic surgery

      1. Surgical approach. The approach used for ascending aortic surgery is a midline sternotomy.

      2. Cardiopulmonary bypass. Because of the proximal involvement of the aorta and because the surgery often includes repair or replacement of the aortic valve, CPB is required.

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

        2. The usual site of cannulation is the femoral artery. This is required if the entire ascending aorta is involved because an aortic cannula cannot be placed distal to the pathology without jeopardizing perfusion to the great vessels.

        3. Venous cannulation usually can be performed through the right atrium; however, femoral venous cannulation may be necessary if the aneurysm is especially large.

      3. Aortic valve involvement. Frequently, either aortic valvuloplasty or aortic valve replacement is necessary with ascending aortic dissections or aneurysms. Which procedure is used depends on the degree of involvement of the sinuses of Valsalva and the aortic annulus.

      4. Coronary artery involvement. With an acute dissecting hematoma, the coronary arteries may be involved. Coronary occlusion usually takes the form of compression of the coronary lumen by the expanding false lumen and will require bypass grafting. Displacement of the coronary arteries from their normal position with enlargement of the aortic annulus will require reimplantation of their orifices into the graft wall or a vein bypass.

      5. Surgical techniques. An example of the usual cross-clamp placement used in surgery of the ascending aorta is shown in Figure 24.4. Note that placement of the distal clamp is more distal than would be the case for simple cross-clamping for coronary surgery and at times might even 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 instead of the coronaries, causing distention of the LV and loss of the myocardial preservative effects of cardioplegia. For these reasons, an immediate aortotomy must be performed and the coronary vessels infused individually with cold cardioplegia. Many centers use retrograde coronary perfusion for cardioplegia administration as an alternative technique to obviate this problem.

        FIG. 24.4 Circulatory support and clamp placement for surgery of the ascending aorta. Femoral arterial cannula usually is required, and distal clamp must be beyond the extent of pathology. Proximal clamp would be needed to provide cold cardioplegia to the aortic root, but placement of this clamp is not possible if the proximal aorta is involved. CPB, cardiopulmonary bypass. (From Benumof JL. Intraoperative considerations for special thoracic surgery cases. In: Benumof JL, ed. Anesthesia for thoracic surgery. Philadelphia: WB Saunders, 1987:384, with permission.)

        If the aortic valve and annulus both are normal, the diseased section of aorta is replaced with graft material. If the annulus is normal and the valve is incompetent, the valve may be resuspended or replaced. If both valve incompetence 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 the composite graft and may not require reimplantation when separate aortic valve replacement and grafts are used, depending on whether enough of the native sinus of Valsalva remains (Fig. 24.5). The posterior wall of the old aneurysm can be wrapped around the graft material and sewn in place to maximize hemostasis.

        FIG. 24.5 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. A section of the aorta that includes the intimal tear is excised, and the edges of the true and false lumens are sewn together. A section of graft is used to replace the excised portion of the aorta.

      6. Complications. Complications are those that occur with any procedure involving CPB and an open ventricle and include the following:

        1. Air emboli

        2. Atheromatous or clot emboli

        3. LV dysfunction secondary to ischemia

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

        5. Renal or respiratory failure

        6. Clotting abnormalities

        7. Surgical hemostasis; bleeding from suture lines can be especially difficult to control.

    4. Anesthetic considerations for ascending aortic surgery

      1. Monitoring

        1. Arterial catheter placement. Because the right subclavian artery may be involved in either the disease process or the surgical repair, a left radial or femoral arterial catheter is inserted for monitoring BP.

        2. ECG. Five-lead, calibrated ECG should be used to monitor both leads II and V5.

        3. PA catheter. Because of the advanced age of many of these patients and the presence of severe systemic disease, a PA catheter can be a useful aid in management preoperatively and postoperatively, but it is not mandatory.

        4. Two-dimensional echocardiography. In addition to its preoperative diagnostic importance, TEE is a useful adjunct in the intraoperative management of these patients. The diagnosis of hypovolemia, hypocontractility, myocardial ischemia, intracardiac air, and valvular dysfunction can be made with TEE. Caution should be exercised when placing this probe in the presence of a large ascending aortic aneurysm.

        5. Neurologic monitors

          1. Electroencephalogram. For evaluating brain function, either raw or processed electroencephalographic data may be helpful for judging the adequacy of cerebral perfusion during CPB. Newer monitors such as the bispectral index may help to assess the depth of anesthesia during these procedures.

          2. Temperature. When correctly placed, a nasopharyngeal temperature probe gives the anesthesiologist an approximation of brain temperature. Rectal temperature also should be monitored.

        6. Renal monitors. As with all cases involving bypass, urine output should be monitored.

      2. Induction and anesthetic agents. See Table 24.9.

      3. Cooling and rewarming. Hypothermic CPB is used in most cases of ascending aneurysms. Deep hypothermic circulatory arrest (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 probably will delay cooling and rewarming, because lower blood flows are used to avoid excessive arterial line pressures. Extra time for cooling and rewarming must be allowed in this setting.

    5. Aortic arch surgery

      1. Surgical approach. The aortic arch is approached through a median sternotomy.

      2. Cardiopulmonary bypass. CPB is required, and femoral cannulation must be used in almost all cases.

      3. Technique. Typical placement of clamps for this procedure is shown in Figure 24.6. Note that the surgical technique dictates that the cerebral vessels be clamped to resect the aneurysmal or dissected section of aortic arch.

        FIG. 24.6 Representation of cannula and clamp placement for surgery of the aortic arch. 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. CPB, cardiopulmonary bypass. (From Benumof JL. Intraoperative considerations for special thoracic surgery cases. In: Benumof JL, ed. Anesthesia for thoracic surgery. Philadelphia: WB Saunders, 1987:384, with permission.)

        The attachments of the arch vessels usually are excised en bloc so that all three vessels are located on one "button" of tissue, as shown in Figure 24.7. This facilitates rapid reimplantation of vessels and reestablishment of blood flow. Once the distal anastomosis is completed, the surgeon sutures the button of arch vessels to the graft material. The clamp can be replaced more proximally, the arch portion of the graft de-aired, the distal aortic clamp removed, and flow reestablished to the cerebral vessels from the femoral CPB aortic cannula. Thus, the time of brain ischemia is minimized. The proximal anastomosis then is completed.

        FIG. 24.7 Aortic arch replacement. A: The distal suture line is completed first, followed by (B) reattachment of the arch vessels. C: Flow is reestablished 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. Resection of aortic arch aneurysms involves interruption or alteration of cerebral blood flow. Various surgical techniques have been used to prevent cerebral ischemia. All involve cooling the brain to reduce metabolic rate and the buildup of toxic metabolites.

        1. DHCA has been adopted by many surgeons as a technically advantageous way to repair aortic arch pathology, because blood flow is stopped and exposure maximized. DHCA requires core cooling to 15° to 22°C, depending on the exact technique used. Turning off the pump and partially draining the patient's blood volume into the pump provide a bloodless field with hypothermic brain protection for up to 45 minutes. This has improved results but is associated with longer bypass runs.

        2. Because of the time limits inherent with DHCA, some groups began using DHCA in conjunction with retrograde cerebral perfusion (RCP) through the superior vena cava as a method of brain protection. This technique has gained acceptance in many centers because it prolongs the "safe time" allowed for what can be a complicated reconstruction of the aortic arch and its vessels. Advantages of RCP include uniform cooling, efficient de-airing 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 [4].

        3. Another technique that has been used with success is continuous anterograde cold blood cerebral perfusion. With this technique, the brain is selectively perfused via the brachiocephalic arteries with cold blood (6° to 12°C) while the patient is maintained at moderate core temperature. As shown in Figure 24.8, the cerebral perfusate is derived from the oxygenator and distributed via a separate roller pump, much the same as anterograde blood cardioplegia. This technique has largely supplanted the older technique of individual cannulation and perfusion of the carotid vessels because of technical considerations. Anterograde perfusion takes advantage of autoregulation of cerebral blood flow, which is thought to remain intact even at low temperature. With intact autoregulation, physiologic protection against ischemia of hyperperfusion will be active. One of the chief advantages of this technique is that DHCA is required only for completion of the distal anastomosis. Because of these advantages, some groups believe that continuous anterograde perfusion is the safest method of brain protection during aortic arch surgery [5].

          FIG. 24.8 Perfusion circuit for anterograde cerebral perfusion for aortic arch surgery. Venous blood from the right atrium drains to the oxygenator (Ox), and 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.)

      5. Complications. Complications from this operation are similar to those with any procedure using CPB. Irreversible cerebral ischemia is a distinct possibility with this type of surgery. Hemostatic difficulties may be increased secondary to the multiple suture lines and long bypass time.

    6. Anesthetic considerations for aortic arch surgery

      1. Monitoring

        1. Arterial BP. An intraarterial catheter can be placed in either the right or left radial artery for prebypass management if the innominate or left subclavian arteries, respectively, are not involved. If both are involved, the femoral artery should be catheterized.

        2. Neurologic monitors

          1. Electroencephalography can be useful not only for ensuring that adequate cooling has been achieved but also for titration of the thiopental dose for brain protection.

          2. Nasal temperature will verify adequate brain cooling.

        3. Transesophageal echocardiography. TEE provides useful information similar to that for ascending aortic surgery (see Section IV.D.1), but care should be taken when placing the probe.

      2. Choice of anesthetic agents. See Table 24.9.

      3. Management of hypothermic circulatory arrest. The technique involves core cooling to 15° to 20°C, packing the head in ice, using other cerebral protective agents, avoiding glucose-containing solutions, and using proper monitoring. More details are provided in Chapter 23.

      4. Complications. Complications related to anesthesia for this procedure are uncommon. One is myocardial depression secondary to the use of thiopental for cerebral protection, and inotropic agents may be needed to wean the patient from CPB.

    7. Descending thoracic aortic surgery

      1. Surgical approach. Exposure of the descending aorta is accomplished through a left thoracotomy incision, usually between the fourth and fifth ribs. A double intercostal incision may be necessary for complete exposure (Fig. 24.9). The patient is placed in a full right lateral decubitus position with the hips slightly rolled to the left to allow access to the femoral vessels. When positioning the patient, it is important to provide protection to pressure points, including use of axillary roll, pillows between the knees, and pads for the head and elbows. It is important to maintain the occiput in line with the thoracic spine to prevent traction on the brachial plexus.

        FIG. 24.9 Surgical approach to an extensive aneurysm or dissection involving the descending thoracic aorta. A single musculocutaneous incision and a double intercostal incision are used. The standard proximal and distal intercostal incisions are made through the fourth and seventh intercostal spaces (ICS), respectively. A traumatic aortic rupture at the isthmus usually can be reached through a single intercostal incision. (From Cooley DA, ed. Surgical treatment of aortic aneurysms. Philadelphia: WB Saunders, 1986:63, with permission.)

      2. Surgical techniques. Whether an aneurysm, dissection, or rupture is being treated, the surgical technique involves placing cross-clamps above and below the lesion, opening the aorta, and replacing the diseased segment with a graft.

        1. Simple cross-clamping. Many groups report success with cross-clamping the aorta above and below the lesion without adjuncts to maintain distal perfusion. This technique has the advantage of simplifying the operation and reducing the amount of heparin needed (Fig. 24.10).

          FIG. 24.10 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: WB Saunders, 1987:384, with permission.)

          Clamping the descending aorta produces marked hemodynamic changes: profound hypertension in the proximal aorta and hypotension below the distal clamp. The increase in afterload that occurs when the majority of the cardiac output goes only to the great vessels causes acute elevations in LV filling pressures and a progressive fall in cardiac output. The presumption is that LV failure will result if this afterload is maintained for any significant length of time. The acute increase in pressure proximal to the clamp can precipitate a catastrophic cerebral event (e.g., rupture of a cerebral aneurysm).

          Mean arterial pressure distal to the cross-clamp decreases to less than 10% to 20% of control. This decrease is paralleled by a decrease in renal blood flow and spinal cord blood flow. The presence of a chronic obstruction to flow and the resultant well-developed collateral flow (i.e., coarctation) will lessen the hemodynamic changes that usually are seen. Examples of BPs above and below a cross-clamp from a series of patients with different aortic pathologies are listed in Table 24.10.

          The use of an "open" technique of simple aortic cross-clamping has been advocated. With this technique, no distal cross-clamp is used, thereby allowing direct inspection of the distal aorta for thrombus or debris. More importantly, graft material can be anastomosed in an oblique fashion that incorporates the maximal number of intercostal arteries.

        2. Shunts. A method that provides decompression of the proximal aorta and perfusion of the distal segment involves placement of a heparin-bonded (Gott) extracorporeal shunt from the LV, aortic arch, or left subclavian artery to the femoral artery (Fig. 24.11). Systemic heparinization is not required. The advantage with this technique is that distal perfusion can be maintained while decompression of the proximal aorta is achieved. The major problems with this technique are technical difficulties with placement and kinking with inadequate distal flows. Two sizes of these shunts are available: 7 mm (5-mm inner diameter) and 9 mm (6-mm inner diameter). The limitations on flow imposed by these relatively small diameters interfere with the actual proximal ventricular decompression and augmentation of distal perfusion pressure that can be achieved.

          FIG. 24.11 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: WB Saunders, 1987:384, with permission.)

        3. Extracorporeal circulation. Historically the first method used for distal perfusion and proximal decompression, extracorporeal circulation (ECC) is being used more often after a period of being out of favor at many centers. There are several ways to perform ECC; all involve removal of blood, passage of blood to an extracorporeal pump, and reinfusion of blood into the femoral artery to perfuse the aorta below the distal cross-clamp (Fig. 24.12). Blood can be returned to the pump from the femoral vein, which is technically the easiest site to use. However, this site requires placement of an oxygenator in the circuit. Alternatively, the left atrium or LV apex may be cannulated for blood return to the pump. The pump may be a standard double roller (positive displacement) or a centrifugal (kinetic) type.

          FIG. 24.12 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 left ventricle 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: WB Saunders, 1987:384, with permission.)

          Each of these variations has disadvantages. Use of an oxygenator requires complete systemic heparinization, which is associated with increased incidence of hemorrhage, especially into the left lung. Left atrial or ventricular cannulation without an oxygenator may allow use of less heparin but carries an increased risk of air embolism. Table 24.11 summarizes the possible cannulation sites and major differences between heparinized shunts and ECC for distal perfusion.

      3. Complications of repair

        1. Cardiac. Cardiac disorders (myocardial infarction, dysrhythmia, or low-output syndrome) are a significant (20% to 40%) cause of death in patients with all types of descending aortic repair.

        2. Hemorrhage. This is a common cause of death (20% to 30%) in all types of repair of the descending aorta.

        3. Renal failure. The incidence of renal failure ranges from 4% to 9% among survivors, with a much higher incidence among nonsurvivors. The etiology is presumed to be a decrease in renal blood flow during aortic cross-clamping. However, renal failure may occur in the presence of apparently adequate perfusion (heparinized shunt or ECC). Preexisting impairment of renal blood flow from a dissection involving the renal arteries increases the incidence of renal failure.

        4. Paraplegia. Most case reviews report the incidence of paraplegia as being in the range from 6% to 10%. [6] This is probably the most devastating morbid event because it is irreversible. The cause is either interruption or prolonged hypoperfusion (more than 30 minutes) of the blood supply to the anterior spinal artery. The anterior spinal artery is formed from the vertebral arteries rostrally. As it descends, it also receives blood from radicular arteries, which arise from the intercostal arteries (Fig. 24.13). In a majority of patients, one of these radicular arteries, the great radicular artery (of Adamkiewicz), contributes a major portion of the supply to the midportion of the anterior spinal artery. Unfortunately, this vessel is almost impossible to identify angiographically or by inspection at operation. It may arise anywhere from T5 to below L1. These anatomic considerations place blood flow in this artery at higher risk intraoperatively and postoperatively. Interruption of flow in this vessel may lead to paraplegia, depending on the contribution available from other collaterals. An anterior spinal syndrome can result, in which motor function is lost (anterior horns) but some sensation remains intact (posterior columns).

          FIG. 24.13 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: WB Saunders, 1986:92, with permission.)

        5. Miscellaneous. Many other complications may arise. Some are a function of the type of pathology. For example, death from multiple organ trauma is a major factor in patients who survive traumatic rupture. Respiratory failure alone and as a component of multiple organ failure is more common with thoracic aortic disease than with abdominal aortic disease. Cerebrovascular accidents are seen in a small number of patients, as is left vocal cord paralysis due to recurrent laryngeal nerve damage.

    8. Anesthetic considerations in descending aortic surgery

      1. General considerations. Anesthesia for descending aortic surgery can be one of the most demanding cases because of the profound changes in numerous organ systems. This topic is summarized in several good reviews [7,8].

      2. Monitoring

        1. Arterial BP. A right radial or brachial arterial catheter is needed to monitor pressures above the cross-clamp because the left subclavian artery may be compromised by the cross-clamp. To assess perfusion distal to the lower aortic clamp, many anesthesia and surgical teams prefer to monitor pressure below the clamp also, which requires placement of a femoral arterial catheter. Should a partial bypass technique be used, the left femoral artery is cannulated for distal perfusion and the right femoral artery is used for BP monitoring.

        2. Ventricular function. Some operative teams prefer to monitor LV function during proximal cross-clamping and therefore insert a PA catheter to follow filling pressures and cardiac output.

        3. Other monitors. Additional monitors used are similar to those used for other thoracic procedures: ECG (standard lead V5 cannot be used because of the surgical approach), pulse oximetry, core temperature, and urine output. TEE would be useful to assess ventricular function and filling volumes during these cases, but anatomic interference by the probe in the surgical field may preclude its use.

      3. One-lung anesthesia. Double-lumen endobronchial tubes are recommended not only to improve surgical exposure but also to provide an element of patient safety. By collapsing the left lung, trauma to that lung is decreased. If manipulation during surgery causes hemorrhage into the airway, the contralateral (right) lung is protected from blood spillage. A left-sided tube is technically easier to place and is used often, but it may be impossible to insert in some patients because of aneurysmal distortion of the trachea or left main stem bronchus. Patients with aortic rupture may have a distorted left main stem bronchus. Right-sided tubes may be used, but proper alignment with the right upper lobe bronchus should be checked with a fiberoptic bronchoscope. Alternatively, tubes with an endobronchial blocker should be considered in cases where adequate placement of a double-lumen tube cannot be achieved. For a detailed description of double-lumen or endobronchial blocker tube placement and single-lung ventilation, see Chapter 25.

      4. Conduct of anesthesia before and during cross-clamping. Before the aorta is cross-clamped, mannitol (0.5 g/kg) should be infused to provide some renal protection during clamping. Even though a shunting procedure will be used, changes in the distribution of renal blood flow make mannitol administration prudent. In addition, sodium nitroprusside should be mixed and ready for infusion.

        After the clamp is applied, it is important to closely monitor acid–base status with serial arterial blood gas measurements. It is common for metabolic acidosis to develop due to hypoperfusion of critical organ beds, and this should be treated aggressively if the patient is normothermic. If simple cross-clamping without adjuncts is used, proximal hypertension should be controlled, again with the realization that distal organ flow may be diminished. In treating proximal hypertension, regional blood flow studies have shown that nitroprusside infusion may decrease renal and spinal cord blood flow in a dose-related fashion. Ideally, cross-clamp time (regardless of technique) should be less than 30 minutes, because the incidence of complications, especially paraplegia, begins to increase above this limit.

        If a heparinized shunt has been placed and proximal hypertension cannot be treated without producing subsequent distal hypotension (less than 60 mm Hg), the surgeon should be made aware that there may be a technical problem with shunt placement. If partial bypass (ECC) is used, the pump speed or venous return can be adjusted so that control of proximal hypertension can be maintained by adequate unloading while the lower body is simultaneously perfused. Usually little or no pharmacologic intervention is necessary in this case because the pump speed and manipulation of venous return provide rapid control of proximal and distal pressures. Table 24.12 lists the treatment options for several clinical scenarios during ECC.

        Before removal of the cross-clamp, a vasopressor should be available. The anesthesiologist must be constantly aware of the stage of operation so that major events such as clamping and declamping may be 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 severe hypotension or myocardial depression. There are several theoretical causes of this declamping syndrome, including washout of acid metabolites, vasodilator substances, sequestration of blood in the lower extremities, and reactive hyperemia. The usual cause, however, is relative or absolute hypovolemia. To attenuate the effects of clamp removal, in the 10 to 15 minutes before unclamping of the thoracic aorta, the volume status of the patient should be optimized. This includes elevating filling pressures by infusing blood products, colloid, or crystalloids. Some advocate prophylactic bicarbonate administration just before clamp removal to minimize the myocardial depression caused by the acidosis that occurs following removal. It is advisable for the surgeon to release the cross-clamp slowly over a period of 1 to 2 minutes to allow enough time for compensatory changes to occur.

        Vasopressors may be needed to compensate for hypotension but must be used with care because even transient hypertension may result in significant bleeding. With a volume-loaded patient and slow clamp release, any significant hypotension usually is short lived and well tolerated. If hypotension is severe, the easiest maneuver is reapplication of the clamp to allow further volume infusion.

        If shunts or ECC is used, declamping hypotension usually is attenuated because the vascular bed below the clamp is less "empty." ECC also provides a means of rapid volume infusion if a reservoir is used.

      6. Fluid therapy and transfusion. Even patients undergoing elective repair of a descending aneurysm may be relatively hypovolemic, and fluid therapy should have the following aims: correct this fluid deficit, provide maintenance fluids, compensate for evaporative and "third space" losses, decrease red cell loss by mild hemodilution, and replace blood loss as needed.

        Despite proximal and distal control of the aorta, blood loss can be considerable in these cases due to back-bleeding from the intercostal arteries. These collateral vessels often are ligated on opening the aorta. Use of cell-scavenging devices has become common and has reduced the need for banked blood, but because massive losses may occur, banked blood may still be needed. As long as liver perfusion is adequate, even with a large blood loss, citrate toxicity usually is not a problem because of rapid "first pass" metabolism in the liver. Repair of a thoracic aneurysm with simple clamping, however, presents a unique situation—the liver is not perfused. In this circumstance, transfusion of large amounts of banked blood may rapidly produce citrate toxicity, resulting in myocardial depression that requires calcium chloride infusion.

CASE 12: Thoracoabdominal Aortic Aneurysms

Serle K. Levin

A 65-year-old man with a long history of smoking and hypertension presents with sharp, tearing back pain for the past 24 hours. He has also complained of worsening cough, wheezing, and dyspnea over the last 3 months.

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  1. Medical Disease and Differential Diagnosis
    1. What are the causes of aortic aneurysms?

    2. How would you classify dissecting aneurysm?

    3. Classify thoracoabdominal aortic aneurysms (TAAAs).

    4. What medical management is appropriate to minimize further compromise?

    5. What coexisting diseases accompany thoracic aortic aneurysms?

    6. What factors are associated with the risk of rupture?

  2. Preoperative Evaluation and Preparation
    1. What organ systems require evaluation and optimization before surgery?

    2. What tests can provide the best diagnosis and most information for this patient?

    3. What major organ systems are threatened by repair of a thoracic aortic aneurysm?

    4. Describe the blood supply of the spinal cord.

    5. How do you detect spinal cord ischemia?

    6. What are the effects of anesthetics on somatosensory evoked potentials (SSEPs) in humans?

    7. What preparations can be made to protect the spinal cord when the descending aorta is cross-clamped?

    8. What preparations can be made to limit kidney damage?

    9. What preparations can be made to maximize pulmonary and cardiac function?

  3. Intraoperative Management
    1. What monitoring would be appropriate for this patient?

    2. What intravenous access would be necessary for this surgery?

    3. What support is necessary from the blood bank?

    4. What type of anticoagulation is used for these cases? What can be done to minimize blood transfusion?

    5. How does the surgeon approach the repair? What types of extracorporeal perfusion can be used?

    6. What physiologic and metabolic alterations do you expect during the surgery related to the cross-clamp?

    7. What can be done to minimize the adverse effects of aortic cross-clamping before placement of the clamp?

    8. What are the adverse effects of aortic unclamping?

    9. What can be done to minimize the adverse effects of aortic unclamping?

    10. How would you approach the anesthetic in this case?

  4. Postoperative Management
    1. What postoperative complications can you anticipate?

A. Medical Disease and Differential Diagnosis

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A.1. What are the causes of aortic aneurysms?

  • Atherosclerosis

  • Aortic dissection

  • Collagen vascular disease

    • Marfan's syndrome

    • Ehlers-Danlos Syndrome

  • Trauma

  • Cystic medial degeneration

  • Infectious

    • Bacterial

    • Viral

    • Spirochete (syphilitic)

    • Fungal

  • Inflammatory

    • Takayasu arteritis

    • Polyarteritis

Back to Quick Links

Kaplan JA, Reich DL, Konstadt SN, Cardiac anesthesia4th ed. Philadelphia: WB Saunders, 1999:826–827.

Kouchoukos NT. Dougenis D. Surgery of the thoracic aorta. N Engl J Med 1997:336:1876–1889.

A.2. How would you classify dissecting aneurysm?

The term dissecting aneurysm is a misnomer, because the condition is not an aneurysm but an aortic dissection, a dissection of the aortic wall. An aneurysm develops when elastica of the aorta is weakened so that the pressure of blood causes dilation of the wall. Aortic dissections result from cystic medial necrosis with mucoid and cystic degeneration of the elastic fibers in the medial of the aorta. Currently, there are two classifications for aortic dissections. Aortic dissection is classified by DeBakey and associates according to the site of origin and the extent of distal dissection, as shown in Fig. 12.1:

  • Type I dissection begins in the ascending aorta near the aortic valve and extends throughout the aorta down to the common iliac arteries. Unfortunately, this is a common type of aortic dissection.

  • Type II dissection is limited to the ascending aorta. This is commonly seen in Marfan's syndrome. This is the rarest form of dissection.

  • Type IIIa dissection begins distal to the left subclavian artery and ends in the descending thoracic aorta. Its localized nature makes it accessible to surgical excision if needed.

  • Type IIIb dissection begins distal to the left subclavian artery and extends into the abdominal aorta. Type IIIb dissections rarely require surgical intervention.

Figure 12.1. Different types of aortic dissection.

Based on clinical course and surgical significance, Daily at Stanford reclassified dissections into two types:

  • Type A dissection originates in the ascending aorta and includes DeBakey's type I and type II dissections.

  • Type B dissection originates only in the descending aorta and is equivalent to DeBakey's type III dissection. These may dissect retrograde into the aortic arch or ascending aorta.

Back to Quick Links

Crawford ES. The diagnosis and management of aortic dissection. JAMA 1990:264:2537–2541.

Daily PO. Trueblood H. Stinson E, et al.Management of acute aortic dissections. Ann Thorac Surg 1990:10:237–247.

DeBakey ME. Cooley DA. Crawford ES, et al.Aneurysms of the thoracic aorta. J Thorac Surg 1958:36:393–420.

O'Connor CJ. Rothenberg DM. Anesthetic considerations for descending thoracic aortic surgery: part I. J Cardiothorac Vasc Anesth 1995:9:581–588.

O'Connor CJ. Rothenberg DM. Anesthetic considerations for descending thoracic aortic surgery: part II. J Cardiothorac Vasc Anesth 1995:9:734–749.

Schwartz SI, Principles of surgery6th ed. New York: McGraw-Hill, 1994:915–916.

A.3. Classify thoracoabdominal aortic aneurysms (TAAAs).

Crawford described four configurations of thoracoabdominal aneurysms (Fig. 12.2):

  • Type I originates below the left subclavian artery and extends to the celiac axis and mesenteric arteries.

  • Type II involves the same areas as Type I but extends caudally to include the infrarenal aorta. It can extend through the abdominal aorta to the iliac bifurcation.

  • Type III begins in the lower descending thoracic aorta (T6) and involves the remainder of the aorta.

  • Type IV begins at the diaphragm and involves the entire abdominal aorta.

Figure 12.2. The Crawford classification of thoracoabdominal aortic aneurysms is defined by anatomic location and the extent of involvement. (From Crawford ES. The diagnosis and management of aortic dissection. JAMA 1990;264:2537–2547, with permission.)

The classification of aneurysm correlates with incidence of perioperative complications and duration of surgery, with Type II having the worst overall outcome and longest duration of surgery.

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Crawford ES. Crawford JL. Safi HJ, et al.Thoracoabdominal aneurysms: preoperative and intraoperative factors determining immediate and long-term results in 605 patients. J Vasc Surg 1986:3:389–404.

A.4. What medical management is appropriate to minimize further compromise?

Immediate preoperative management is crucial in establishing stability in this patient. In the case of a dissecting aneurysm, well-controlled blood pressure and decreased contractility can limit the extension of the dissection. In the scenario of a leaking aneurysm, the same hemodynamic principles apply. Control of blood pressure, particularly limiting abrupt changes in pressure, diminish the stress forces impacting on the wall of the aneurysm. In addition, reducing contractility and thereby the force of contraction of the left ventricle, can help reduce the spread of the dissection or extent of leak. The best methods to accomplish these objectives are through aggressive antihypertensive management and -receptor antagonism. Use of a pure vasodilator can result in a decrease in afterload but can increase cardiac output and cause reflex tachycardia. These two side effects are undesirable. A -receptor antagonist can offset both of these effects.

Ruptured aneurysms present in shock. Volume resuscitation and surgical containment of the rupture are the only hope for survival.

Back to Quick Links

Crawford ES. The diagnosis and management of aortic dissection. JAMA 1990:264:2537–2547.

Kouchoukos NT. Dougenis D. Surgery of the thoracic aorta. N Engl J Med 1997:336:1876–1889.

A.5. What coexisting diseases accompany thoracic aortic aneurysms?

Cardiovascular and pulmonary disease most often accompany thoracic aneurysms. Hypertension is present in 70% of patients and coronary artery disease (CAD) in almost 50%. The prevalence of smoking is high in thoracic vascular surgery patients. Chronic obstructive pulmonary disease (COPD) is seen in 34% of patients.

Renal insufficiency is also common. Diabetic nephropathy and hypertension induced renal disease can compromise renal function. Atherosclerotic disease of the abdominal aorta or renal arteries often compounds these problems.

Back to Quick Links

LeMaire SA. Miller CC. Conklin LD, et al.A new predictive model for adverse outcomes after elective thoracoabdominal aortic aneurysm repair. Ann Thorac Surg 2001:71:1233–1238.

A.6. What factors are associated with the risk of rupture?

The size and rate of expansion of the aneurysm are two well-documented predictors of aneurysm rupture. A diameter of greater than 5 cm and a growth rate of 1 cm annually are criteria for surgical intervention.

Certain concomitant diseases predict an increased risk of rupture, such as smoking and COPD. The average annual increase in aneurysm size is faster in smokers than in nonsmokers. COPD exceeds smoking as a risk factor for rupture of both the thoracic and abdominal aorta.

Other factors that increase the risk of rupture are advancing age and pain.

Hypertension, although correlating with the development of aneurysms, has not been conclusively shown to increase the risk of rupture. Renal failure has been shown in most, but not all, predictive studies to correlate with increased risk of rupture.

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Dapunt OE. Galla JD. Sadeghi AM, et al.The natural history of thoracic aortic aneurysms. J Thorac Cardiovasc Surg 1994:107:1323–1333.

Griepp RB. Ergin MA. Galla JD, et al.Natural history of descending thoracic and thoracoabdominal aneurysms. Ann Thorac Surg 1999:67:1927–1930.

Juvonen T. Ergin MA. Galla JD, et al.Prospective study of the natural history of thoracic aortic aneurysms. Ann Thorac Surg 1997:63:1533–1544.

B. Preoperative Evaluation and Preparation

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B.1. What organ systems require evaluation and optimization before surgery?

The patient's coexisting diseases, the organs affected by the expanding aneurysm and by the surgical approach should all be assessed before surgery. Because these aneurysms present emergently in many cases, a short battery of tests can assist in gauging organ function.

Evaluation of ventricular function and myocardial ischemia is crucial to survival in the operating room. Repairing thoracoabdominal aneurysms without the support of cardiopulmonary bypass (CPB) puts remarkable strain on myocardial function and coronary blood supply. Adequate knowledge of preoperative ventricular function, valvular function, and coronary anatomy can guide hemodynamic management and surgical decision making throughout the case. The elective patient with symptoms or changes on the electrocardiogram consistent with myocardial ischemia or infarction should undergo a stress test and, if necessary, coronary angiography. Angioplasty or coronary bypass surgery should be performed in those patients with clinically significant CAD.

Because one-lung ventilation is essential for surgical exposure, severe pulmonary disease can make a repair without full CPB impossible. Patients with poor diffusing capacity or severe COPD cannot survive one-lung ventilation. Full CPB would be required to complete the repair of a thoracic aneurysm in these patients but it can have detrimental effects on their already poor pulmonary function. Postoperative respiratory failure is the leading cause of mortality in patients undergoing thoracic aortic aneurysm repair.

Renal function must be assessed because the kidneys are subjected to a significant ischemic insult during surgery. Perioperative renal failure has a notable effect on overall survival.

Back to Quick Links

Kaplan JA, Reich DL, Konstadt SN, Cardiac anesthesia4th ed. Philadelphia: WB Saunders, 1999:835–839.

Kouchoukos NT. Dougenis D. Surgery of the thoracic aorta. N Engl J Med 1997:336:1876–1889.

B.2. What tests can provide the best diagnosis and most information for this patient?


Magnetic resonance imaging (MRI), computed tomography (CT) scan, or angiography of the aorta define the extent of aortic disease including involvement of carotid, subclavian, renal, and mesenteric arteries. Often, angiography can locate the artery of Adamkiewicz, helping surgeons to reimplant the artery during the repair.


Electrocardiogram (ECG) provides quick and accurate information about ongoing ischemia and infarction. More definitively, transesophageal echocardiography (TEE) can quickly ascertain information relating to ventricular and valvular function. It allows direct visualization of the distal aortic arch and descending thoracic aorta to assess extent of disease, thrombus, or dissection. It can also detect pericardial and pleural fluid collections that can be seen with ruptured or leaking aneurysms. TEE is useful during the surgical procedure to monitor ventricular volume and the occurrence of ischemia. As mentioned previously, the elective surgical candidate with clinical or ECG evidence of ischemia or infarction warrant a stress test and, possibly, angiography. Preoperative cardiac catheterization can determine coronary stenosis that can be treated before elective surgical repair.


Preoperative pulmonary function tests, including arterial blood gas analysis, are useful to assess resting lung function and to predict the ability of the patient to tolerate single-lung ventilation.


Hemoglobin, hematocrit, and platelet count are important to gauge transfusion requirements during the surgical repair. Blood urea nitrogen and creatinine levels can reveal an acute change in renal function or provide evidence of chronic renal insufficiency.

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Cigarroa JE. Isselbacher EM. DeSanctis RW, et al.Diagnostic imaging in the evaluation of suspected aortic dissection—old standards and new directions. N Engl J Med 1993:328:35–43.

Kouchoukos NT. Dougenis D. Surgery of the thoracic aorta. N Engl J Med 1997:336:1876–1889.

B.3. What major organ systems are threatened by repair of a thoracic aortic aneurysm?

For all of the organ systems affected by the surgery, the most significant threat to organ function and survival is the duration of the aortic cross-clamp. It is during this time that flow is either halted to the organs or they are subjected to their maximal stress. The duration of clamping is related to the surgeon, surgical technique, and classification of aneurysm.

Spinal cord

Spinal cord ischemia is one of the major concerns during thoracoabdominal aneurysm repair. Prolonged ischemia of the cord can lead to paraplegia or paraparesis. Several factors contribute to spinal cord ischemia—duration of cross-clamp, preexisting cord ischemia, and variability in spinal arterial supply. Two broad approaches are taken to protect the spinal cord—increase blood supply and/or provide pharmacologic and temperature-related neuroprotection.


Repair of the descending aorta routinely interrupts blood flow to the kidneys and mesentery. As a result, precautions are taken to minimize the occurrence of acute renal failure. In addition, gut ischemia from hypoperfusion can lead to an increase in intestinal permeability and sepsis.


The lung parenchyma is subjected to manipulation, compression, and retraction throughout the surgery. Much of this manipulation occurs after the patient is anticoagulated. Bleeding can occur within the tracheobronchial tree leading to ventilatory difficulties intraoperatively and postoperatively.


Alterations in preload, afterload, and oxygen carrying capacity subject the heart to profound alterations in myocardial oxygen delivery and consumption. As described in more detail later, the heart faces major swings in afterload with placement and removal of the aortic cross-clamp. In addition, abrupt changes in preload resulting from blood loss, cross-clamp placement, and volume resuscitation further strain myocardial oxygen balance and ventricular contractility. Acidosis, hypocalcemia, and alteration in serum potassium can all affect myocardial contractility and conduction.

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O'Conner CJ. Rothenberg DM. Anesthetic considerations for descending thoracic aortic surgery: part I. J Cardiothorac Vasc Anesth 1995:9:581–588.

O'Conner CJ. Rothenberg DM. Anesthetic considerations for descending thoracic aortic surgery: part II. J Cardiothorac Vasc Anesth 1995:9:734–747.

B.4. Describe the blood supply of the spinal cord.

The spinal cord has a system of longitudinal arteries and a system of transverse arteries as shown in Fig. 12.3. Anatomic studies have shown that the most important longitudinal arteries are a single anterior spinal artery supplying 75% of the cord and a pair of posterior spinal arteries supplying 25% of the cord. Although in humans the anterior spinal artery is a continuous vessel, modern anatomy has emphasized the importance of the reinforcing transverse arteries rather than the meager longitudinal vessels. The territory supplied by the anterior spinal artery is divided into three functionally distinct levels: cervicodorsal, intermediate or midthoracic, and thoracolumbar. The cervicodorsal region receives its blood supply from the vertebral, subclavian, thyrocervical, and costocervical arteries. The midthoracic region is supplied by a meager left or right intercostal artery arising between the fourth and the ninth thoracic vertebrae. The thoracolumbar region of the anterior spinal artery receives its blood supply mainly from one of the intercostal arteries called the arteria radicularis magna or the artery of Adamkiewicz. It arises at the level of T5 to T8 in 15%, T9 to T12 in 60%, L1 in 14%, and L2 in 10% of patients. The arteria radicularis magna is often involved in the surgical repair.

Figure 12.3. Diagram to show components of the anterior spinal artery. A: Lateral view. B: Anteroposterior view showing origins of artery of Adamkiewicz. C: Schematic representation of direction and volume of flow from nutrient vessels supplying the anterior spinal artery. Size of arrows is proportional to flow contribution. (From Bromage PR. Epidural anesthesia. Philadelphia: WB Saunders, 1978:50–54, with permission.)

The anterior spinal artery is smaller above than below the entry of the arteria radicularis magna. Resistance to blood flow is 51.7 times greater going up the anterior spinal artery as compared with coming down the artery. Therefore, distal aortic perfusion during thoracic aortic cross-clamping protects the spinal cord below the arteria radicularis magna but not above it. This is why paraplegia still occurs in about 2% to 15% of patients having thoracic aortic surgery with distal aortic perfusion. However, reimplantation of intercostal arteries during surgery has been shown to reduce the incidence of neurologic injury.

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Bromage PR. Epidural anesthesia Philadelphia: WB Saunders, 1978:50–54.

DiChiro G. Fried LC. Doppman JL. Experimental spinal cord angiography. Br J Radiol 1970:43:19–30.

Kaplan JA, Reich DL, Konstadt SN, Cardiac anesthesia4th ed. Philadelphia: WB Saunders, 1999:835–839.

Miller RD, Anesthesia5th ed. Philadelphia: Churchill Livingstone, 2000:1872.

Piccone W. DeLaria GA. Najafi H. Descending thoracic aneurysms. Bergan JJ, Yao JST, Aortic surgery Philadelphia: WB Saunders, 1989:249.

Svensson LG. Richards E. Coull A, et al.Relationship of spinal cord blood flow to vascular anatomy during thoracic aortic cross-clamping and shunting. J Thorac Cardiovasc Surg 1986:91:71–78.

Williams GM. Perler BA. Burdick JF, et al.Angiographic localization of spinal cord blood supply and its relationship to postoperative paraplegia. J Vasc Surg 1991:13:23–33.

B.5. How do you detect spinal cord ischemia?

Evoked potential is used in thoracoabdominal surgery to detect spinal cord ischemia. Two varieties of evoked potential are used in TAAA repair. SSEPs travel through the dorsal root ganglia to the posterior columns of the spinal cord. The potentials continue along the lemniscal pathways on to the thalamus and the cortex. Comparison of the latency and amplitude of the potentials, tested minutes apart, define the degree of change in the SSEP. Temperature, anesthetic depth, and changes in blood flow can alter the evoked potentials. Changes in blood flow through the anterior spinal artery are not reflected in the posterior columns. It is possible, therefore, to have paralysis with normal SSEPs.

Ischemia of the spinal cord is indicated by increases in latency and/or decreases in amplitude of evoked potential tracing. The typical SSEP trace is shown in Fig. 12.4, and its response to aortic cross-clamping is shown in Fig. 12.5. The latency increases as early as 4 minutes following aortic cross-clamping, with progress to cessation of spinal cord conduction within 7 minutes of cross-clamping. Return of spinal cord conduction occurs 47 minutes following distal aortic reperfusion, with return to normal spinal cord conduction within 24 hours after operation. It has been shown that the loss of SSEP signals for longer than 14 to 30 minutes was associated with postoperative neurologic deficit.

Figure 12.4. Typical somatosensory evoked potential trace. (From Cunningham JN Jr, Laschinger JC, Merkin HA, et al. Measurement of spinal cord ischemia during operations upon the thoracic aorta: Initial clinical experience. Ann Surg 1982;196:285–296, with permission.)

Figure 12.5. Somatosensory evoked potential response to aortic cross-clamping (AXC). (From Cunningham JN Jr, Laschinger JC, Merkin HA, et al. Measurement of spinal cord ischemia during operations upon the thoracic aorta: initial clinical experience. Ann Surg 1982;196:285–296, with permission.)

Motor evoked potentials (MEPs) do monitor areas of the cord supplied by the anterior spinal artery. To assess MEPs, patients require partial paralysis and light plane of anesthesia. Both of these requirements are suboptimal anesthetic options for a TAAA repair.

Finally, the signal-to-noise ratio of evoked potentials make interpretation of the data in the operating room more difficult and less reliable.

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Coles JC. Wilson GJ. Sima AF, et al.Intraoperative detection of spinal cord ischemia using somatosensory cortical evoked potentials during thoracic aortic occlusion. Ann Thorac Surg 1982:34:299–306.

Cunningham JN Jr. Laschinger JC. Spencer FC. Monitoring of somatosensory evoked potentials during procedures on the thoracoabdominal aorta: clinical observations and results. J Thorac Cardiovasc Surg 1987:94:275–285.

Ginsbury HH. Shetter AG. Raudzens PA, et al.Postoperative paraplegia with preserved intraoperative somatosensory evoked potentials. J Neurosurg 1985:63:296–300.

Grundy BL. Intraoperative monitoring of sensory-evoked potentials. Anesthesiology 1983:58:72–87.

Meylaerts SA. Jacobs MJ. van Iterson V, et al.Comparison of transcranial motor evoked potentials and somatosensory evoked potentials during thoracoabdominal aortic aneurysm repair. Ann Surg 1999:230:742–749.

B.6. What are the effects of anesthetics on somatosensory evoked potentials (SSEPs) in humans?

Halothane, enflurane, and isoflurane all produce dose-related reductions in the amplitude and increases in the latency of the cortical component of the SSEP. These changes are most pronounced with enflurane and least with halothane. At 1.5 minimum alveolar concentration (MAC) of each volatile agent, cortical latency decreased and amplitude increased when nitrous oxide was discontinued. The results suggest that in neurologically intact patients, end-tidal concentrations of 1.0 MAC halothane and 0.5 MAC enflurane or isoflurane (each in 60% N2O) can be compatible with effective SSEP monitoring. Volatile anesthetic concentrations consistent with satisfactory SSEP recording may be greater if N2O is not used. Bernard et al. has demonstrated that compared with cortical SSEPs, neurogenic MEP signals are well preserved in patients undergoing surgery to correct scoliosis under general anesthesia supplemented with isoflurane or desflurane in concentrations as great as 1 MAC.

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Bernard JM. Pereon Y. Tayet G, et al.Effects of isoflurane and desflurane on neurogenic motor- and somatosensory-evoked potential monitoring for scoliosis surgery. Anesthesiology 1996:85:1013–1019.

Peterson DO. Drummond JC. Todd MM. Effects of halothane, enflurane, isoflurane and nitrous oxide on somatosensory evoked potentials in humans. Anesthesiology 1986:65:35–40.

B.7. What preparations can be made to protect the spinal cord when the descending aorta is cross-clamped?

Hypothermia has been shown to be effective in protecting against organ ischemia. Each degree drop in temperature reduces metabolism by 7%, allowing longer periods of ischemia without significant neurologic sequelae compared with normothermia. Direct spinal cord cooling has also been attempted as a method of prolonging the duration of ischemia before irreversible ischemia occurs.

Attempts to increase arterial blood flow can be directed at increasing blood pressure above the cross-clamp, increasing arterial blood pressure below the clamp, decreasing venous pressure or decreasing the compressive forces surrounding the spinal cord.

Decrease in cord compression can be accomplished with drainage of CSF. Placement of a spinal drain allows monitoring of spinal fluid pressure and the ability to drain fluid when the pressure rises. CSF drainage has been advocated for spinal cord protection. In a recent review, no conclusive data was found to support the use of CSF drainage. Of the many studies that advocate its use, the methodologic and statistical flaws negate the conclusions drawn from them.

Among surgeons, however, CSF drainage appears to be a routine arm of the multifactorial approach to spinal cord protection. Anecdotal reports have been published in which postoperative paraplegia was reversed with placement of a spinal drainage catheter and removal of CSF. In our institution, spinal cord pressure is maintained below 15 mm Hg during and after the period of aortic cross-clamp.

Anastomosis of intercostal or lumbar arteries to the graft has been associated with a lower incidence of spinal cord ischemia.

Naloxone, methylprednisolone, magnesium, and intrathecal papaverine have all been suggested to protect the cord. At this time, no pharmacologic agents have been proven to protect the spinal cord.

Elevated serum glucose leads to poorer neurologic outcome in patients with cerebral ischemia. As a result, tight glucose control has been advocated to limit the damage to the spinal cord.

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Acher CW. Wynn MM. Hoch JR, et al.Combined use of cerebral spinal fluid drainage and naloxone reduces the risk of paraplegia in thoracoabdominal aneurysm repair. J Vasc Surg 1994:2:2–19.

Cambria RP. Davison JK. Zanneti S. Clinical experience with epidural cooling for spinal cord protection during thoracic and thoracoabdominal aneurysm repair. J Vasc Surg 1997:25:234–241.

Gharagozloo F. Neville RF Jr. Cox JL. Spinal cord protection during surgical procedures on the descending thoracic and thoracoabdominal aorta: a critical overview. Sem Thorac Cardiovasc Surg 1998:10:73–86.

Ling E. Arellano R. Systematic overview of the evidence supporting the use of cerebrospinal fluid drainage in thoracoabdominal aneurysm surgery for prevention of paraplegia. Anesthesiology 2000:93:1111–1132.

Von Seggesser LK. Marty B. Mueller X, et al.Active cooling during open repair of thoraco-abdominal aortic aneurysms improves outcome. Eur J Cardiothorac Surg 2001:19:411–416.

B.8. What preparations can be made to limit kidney damage?

Postoperative renal dysfunction is a common occurrence following repair of thoracic and abdominal aortic surgeries. Renal dysfunction is a result of hypoperfusion and renal ischemia during the period of cross-clamping. Adequate blood volume and renal perfusion before and following cross-clamp placement are vital to minimize the overall insult.

Many modalities have been proposed to limit or avoid renal dysfunction. The most direct approach is to provide perfusion to the renal arteries while the upper portions of the aneurysm are resected and replaced. Selective renal perfusion and distal aortic perfusion reduce the period of renal ischemic time and theoretically should decrease the duration of hypoperfusion. Use of a cold renal perfusate induces renal hypothermia and allows the kidneys to tolerate longer periods of hypoperfusion. Pharmacologically, mannitol, furosemide, and low-dose dopamine are used without clear evidence of proven benefit.

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Kaplan JA, Reich DL, Konstadt SN, Cardiac anesthesia4th ed. Philadelphia: WB Saunders, 1999:850–851.

O'Conner CJ. Rothenberg DM. Anesthetic considerations for descending thoracic aortic surgery: part I. J Cardiothorac Vasc Anesth 1995:9:581–588.

O'Conner CJ. Rothenberg DM. Anesthetic considerations for descending thoracic aortic surgery: part II. J Cardiothorac Vasc Anesth 1995:9:734–747.

B.9. What preparations can be made to maximize pulmonary and cardiac function?

Preexisting pulmonary disease and a history of smoking makes these patients more susceptible to intraoperative pulmonary problems. Compounding these diseases is the need for one-lung ventilation throughout the surgery. As a result, intraoperative hypoxemia is a potential problem. Improving the preoperative pulmonary function is the best hope to avoid this problem. Aggressive pulmonary toilet, bronchodilator therapy, and other interventions routinely used to optimize pulmonary function for thoracic surgery are critical.

Proper endotracheal tube or bronchial blocker position allows less physical manipulation and trauma to the left lung by the surgeon.

Anticipation of the hemodynamic alterations imposed by the surgery, including the need to treat ischemia and dysrhythmias rapidly, is the best approach to preserving cardiac function. Appropriate pharmacologic agents should be prepared and available to manage the changes seen in preload, afterload, rhythm, and contractility.

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Kaplan JA, Reich DL, Konstadt SN, Cardiac anesthesia4th ed. Philadelphia: WB Saunders, 1999:851–853.

O'Conner CJ. Rothenberg DM. Anesthetic considerations for descending thoracic aortic surgery: part I. J Cardiothorac Vasc Anesth 1995:9:581–588.

O'Conner CJ. Rothenberg DM. Anesthetic considerations for descending thoracic aortic surgery: part II. J Cardiothorac Vasc Anesth 1995:9:734–747.

C. Intraoperative Management

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C.1. What monitoring would be appropriate for this patient?

Right arm arterial line

A right upper extremity arterial line is placed to assist in the management of TAAAs. The right arm arterial supply is the best for monitoring accurate blood pressure in these patients because the surgical approach can involve the left subclavian artery, rendering left radial and axillary artery pressures inaccurate. Several institutions place an arterial line distal to the cross-clamp in a lower extremity, to assess collateral or distal arterial perfusion. The utility of this additional line seems to be institution dependent.

Pulmonary artery (PA) catheter

A right heart catheter is useful to assess the patient's ventricular filling pressures, cardiac output, and mixed venous saturation throughout the surgery. PA pressures can reflect volume status or indicate acute failure of the left ventricle intraoperatively. Central access allows for the rapid infusion of volume and the administration of vasoactive drugs (i.e., inotropes, vasoconstrictors).


TEE provides a visual assessment of left ventricular (LV) volume and function during the surgery. It can give a more accurate assessment of ventricular filling than the PA catheter. Ischemia is a frequent occurrence during the repair. New alterations in wall motion can help assess the presence and significance of intraoperative ischemia. A view of right ventricle function and most of the ascending aorta are added benefits of TEE. Visualization of the left ventricle can be difficult in the lateral decubitus position when the heart does not overlie the esophagus well.

CSF pressure

CSF pressure increases during TAAA repair presumably because arterial blood pressure exceeds cerebral autoregulation. The increased blood pressure following placement of the cross-clamp results in increased cerebral blood flow that, in turn, is reflected in a higher CSF pressure. In addition, the ischemic spinal cord becomes edematous, expanding in a fixed space. The increase in pressure begins with the placement of the aortic cross-clamp and can rise enough to potentially impinge on the collateral arterial supply to the already ischemic spinal cord. Several authors have suggested that removing spinal fluid and decreasing the external pressure on the cord will allow for more normal collateral flow.


Tight glucose control can have an impact on neurologic outcome. Elevated blood glucose from glucose-containing solutions has been shown to yield poor results in cerebral ischemia compared with normal blood glucose in patients receiving non-glucose-containing solutions. Animal studies have shown a similar effect with spinal cord ischemia.

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Drummond LC. Moore SS. The influence of dextrose administration on neurologic outcome after temporary spinal cord ischemia in the rabbit. Anesthesiology 1989:70:649.

Gharagozloo F. Neville RF Jr. Cox JL. Spinal cord protection during surgical procedures on the descending thoracic and thoracoabdominal aorta: a critical overview. Semin Thorac Cardiovasc Surg 1998:10:73–86.

O'Connor CJ. Rothenberg DM. Anesthetic considerations for descending thoracic aortic surgery: part 1. J Cardiothorac Vasc Anesth 1995:9:581–588.

C.2. What intravenous access would be necessary for this surgery?

Rapid volume resuscitation is a vital component to survival during this surgery. In our institution, two 9 French catheters are placed—one in the right internal jugular vein and one in the right femoral vein—to provide the ability of delivering flow rates near 1,500 mL per minute through a rapid infusion system. Additional intravenous lines are placed for blood product and medication infusions.

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Kaplan JA, Reich DL, Konstadt SN, Cardiac anesthesia4th ed. Philadelphia: WB Saunders, 1999:848.

C.3. What support is necessary from the blood bank?

A major component of the anesthetic approach to this surgery is volume resuscitation. As mentioned previously, considerable intravenous access is required to maintain euvolemia throughout the surgery and compensate for surgical blood loss. To ensure that adequate quantities of packed red blood cell (PRBC), fresh frozen plasma, and platelets are available for use in the operating room, the blood bank must be forewarned about the magnitude of support they will be required to lend. In our institution, we routinely have 8 to 10 units of PRBCs available in the operating room with an additional 6 units available in the blood bank. Four units of plasma and 12 units of platelets are also available.

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Kaplan JA, Reich DL, Konstadt SN, Cardiac anesthesia4th ed. Philadelphia: WB Saunders, 1999:847–850.

C.4. What type of anticoagulation is used for these cases? What can be done to minimize blood transfusion?

Heparin, 100 U/kg, is administered 5 minutes before cross-clamp placement for systemic anticoagulation.

Use of blood salvaging techniques, like Cellsaver, decreases the amount of homologous blood used during the case. The anticoagulant used for this device can be either heparin or citrate. Citrate binds calcium and depending on the quantity of blood processed and returned to the patient, up to 10 g of calcium chloride have been administered to maintain normal ionized calcium levels. If heparin is used to anticoagulate the Cellsaver, protamine sulfate must be administered in amounts larger than anticipated.

Autologous blood can be harvested from the patient before surgery or in the operating room. Occasionally, the procedure can be completed without transfusion of homologous blood or blood products. More often, however, the blood loss is significant enough that PRBC transfusion is necessary. The use of Cellsaver can limit homologous red cell transfusion, but the technique washes out plasma proteins and platelets in the process. The result can be a dilutional coagulopathy and thrombocytopenia necessitating blood product transfusion to correct the problem.

Antifibrinolytics and aprotinin have been used but are not usually recommended.

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Kaplan JA, Reich DL, Konstadt SN, Cardiac anesthesia4th ed. Philadelphia: WB Saunders, 1999:847–850.

C.5. How does the surgeon approach the repair? What types of extracorporeal perfusion can be used?

Approach to the thoracic aorta is through the left chest. The incision extends from above the fifth intercostal space, across the diaphragm, and into the abdomen. A partial lateral decubitus position is required with the chest turned to the right but the hips almost supine to allow cannulation of the femoral vessels.

Single-lung ventilation is necessary to provide adequate visualization of the aorta and its branches. In addition, collapse of the left lung reduces the need for lung retraction, decreasing trauma to the lung parenchyma. A double-lumen endotracheal tube prevents contamination of the right lung in the event of a pulmonary hemorrhage in the left lung. Bronchial blockers or a Univent tube are equally as efficacious. Following completion of the surgery, a double-lumen tube is changed to a single-lumen tube to facilitate postoperative ventilation.

The optimal surgical technique has yet to be defined for this operation and is dependent on the comfort and skill of the surgeon, the extent of the aneurysm, and the coexisting diseases of the patient. Several approaches to extracorporeal circulation have been used to manage these patients intraoperatively in an attempt to minimize the myriad of insults imposed by surgical correction.

Clamp and sew

The clamp and sew technique involves clamping the proximal portion of the descending thoracic aorta and replacing the aneurysm with graft. The distal anastomosis to the lower abdominal aorta is performed without a clamp, allowing the distal aorta to decompress. Many surgeons approach the smaller aneurysms with a clamp and sew technique. The advantage to this approach is avoidance of full systemic heparinization. A time pressure is imposed on the surgeon during this approach because there is no help from a pump to support distal or collateral perfusion.

CPB with deep hypothermic circulatory arrest (DHCA)

CPB using femoral artery and vein cannulation helps support the circulation and allows predictable alterations in temperature. DHCA has been used throughout cardiac surgery to protect organs at risk for significant ischemic injury. In the case of a TAAA, these organs are the kidneys and the spinal cord. In addition, it allows the surgery to proceed in a bloodless field. Advantages of DHCA are the elimination of concerns relating to cardiac and pulmonary function and the lack of hemodynamic alterations associated with the cross-clamp. The advantage of hypothermic protection, however, is offset by the high incidence of postbypass bleeding and transfusion requirements. Additional disadvantages are seen in the usual risks of full CPB and extending the duration of surgery. The choice to use CPB with DHCA is, in most cases, institution dependent. However, when the proximal aorta cannot be clamped without disrupting cerebral blood flow through the left carotid artery, this method must be used to protect the brain from hypoperfusion.

Left atrial-femoral artery (LA-FA) bypass

LA-FA bypass provides distal aortic perfusion with a circuit that removes oxygenated blood from the left atrium and routes it to the descending aorta below the cross-clamp. This redirection of flow decompresses the left ventricle and reduces the blood pressure in the aorta above the proximal cross-clamp. The lower extremity flow allows for perfusion of the legs and possibly improves collateral flow through the lower portions of the anterior spinal artery. The theory behind this approach is the benefit of relying on collateral flow to areas of ischemia. It can reduce developing acidosis seen as a result of the cessation of lower extremity flow during the clamp and sew technique. In addition, lower extremity perfusion maintains a high venous capacitance that diminishes the degree of hypotension that can be seen with release of the aortic cross-clamp. The use of this bypass circuit requires heparinization, but it does not use an oxygenator. Flow through the circuit is dependent on the overall volume state of the patient. The better resuscitated the patient, the higher the allowable flow through the LA-FA circuit. LA-FA bypass is preferred in patients with significant myocardial dysfunction or other systemic diseases and in aneurysms that require extensive surgery and prolonged periods of aortic cross-clamping.

Selective perfusion

Selective perfusion permits arterial flow through the mesenteric and splanchnic circulation. Small catheters are used to cannulate the mesenteric, celiac, and renal arteries. Flow is diverted from the upper aorta and into these arteries to minimize the ischemic time of the gut and kidneys.

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Kaplan JA, Reich DL, Konstadt SN, Cardiac anesthesia4th ed. Philadelphia: WB Saunders, 1999:839–844.

O'Conner CJ. Rothenberg DM. Anesthetic considerations for descending thoracic aortic surgery: part II. J Cardiothorac Vasc Anesth 1995:9:734–747.

C.6. What physiologic and metabolic alterations do you expect during the surgery related to the cross-clamp?


Application of the aortic cross-clamp abruptly increases blood pressure in the upper extremities and drastically lowers blood pressure below the clamp. The increase in blood pressure results from the sudden increase in afterload and vascular resistance. Treatment of hypertension with vasodilators can help improve cardiac function and decrease blood loss. The aim is to return systolic blood pressure to a stable range near 120 mm Hg. Perfusion below the cross-clamp depends on collateral flow and is completely pressure dependent. Preload is initially increased following placement of the clamp through a translocation of blood from the lower extremities to the upper extremities. The major periods of blood loss occur when the aorta is first opened and throughout the time that the anastomosis is sewn in place. This ongoing loss results from arterial collateral flow emptying into the surgical field from the intercostal arteries and from the unclamped segment of the distal aorta. Continuous aggressive volume replacement with crystalloid, colloid, and blood products help attenuate the decrease in preload. Contractility and myocardial oxygen consumption increase in response to the change in loading conditions. A heart with normal function can usually maintain its performance and respond positively to changes in load because it compensates for the increase in myocardial oxygen demand with an increase in coronary blood flow. Hearts with significant CAD are unable to make this adjustment in oxygen delivery and are prone to ischemia. Patients with depressed LV function that cannot improve contractility or myocardial blood flow will decompensate in response to aortic clamping.

Metabolic and humoral

Metabolic acidosis develops and serum lactate levels increase during the period of clamping. The acid load can adversely affect vasomotor tone and cardiac function following declamping. Numerous humoral responses are elicited by the placement and removal of the thoracic cross-clamp. The renin-angiotensin and adrenal axes are activated in response to the stimulus of the aortic cross-clamp. Oxygen free radicals are generated with reperfusion. Prostaglandins, neutrophils, complement, and a host of other mediators are all released or activated during the surgery.


A significant amount of the patient's blood volume can be lost and replaced during the repair. Because of the physiologic demands of the surgery and the preexisting diseases in these patients, oxygen carrying capacity and oxygen delivery are important to the patients' overall survival. An increase in perioperative mortality has been noted in patients with hemoglobin less than 8.0 g/dL during repair of a TAAA. Red cell transfusion is often necessary to maintain adequate hemoglobin. In our experience, it is possible to undergo a complete repair of a TAAA without any homologous blood products, but this is infrequent.


Much of the lung damage seen intraoperatively and postoperatively is from mechanical compression and retraction during the procedure that leads to bleeding. Other sources of pulmonary damage are reflected by an elevation in pulmonary vascular resistance (PVR) and an increase in membrane permeability. These findings are related to placement and removal of the clamp through an increase in pulmonary blood volume and the release of various vasoactive mediators. Prostaglandins, the renin-angiotensin system, the complement cascade, and oxygen free radicals have all been implicated.

C.7. What can be done to minimize the adverse effects of aortic cross-clamping before placement of the clamp?


The potential damage to the kidneys can be limited by avoiding a prerenal injury before clamp placement. If the aneurysm does not mechanically obstruct renal blood flow, volume resuscitation is the best way to accomplish this goal. Various pharmacologic manipulations are begun in anticipation of the aortic cross-clamp. Dopamine (1 to 3 g/kg/minute), mannitol (0.25 mg/kg), and furosemide (up to 1 mg/kg) are administered in the period just before placement of the clamp.


An infusion of sodium bicarbonate (1 to 2 mEq/kg/hour) is maintained for much of the surgery to create a large bicarbonate buffer that will offset the anticipated metabolic acidosis after release of the clamp. A bicarbonate infusion allows a larger than normal buffering capacity to offset the effects of the acidosis. Boluses of bicarbonate can be given but cause a decrease in blood pressure if given quickly.


Sodium nitroprusside or trimethaphan infusions are prepared as arterial vasodilators for blood pressure control during the cross-clamp. Trimethaphan has less of a detrimental effect on spinal cord pressure than sodium nitroprusside. Sodium nitroprusside causes cerebral vasodilatation and a concomitant rise in intracranial and spinal cord pressure. Inhalational anesthetics can be particularly useful as vasodilators. A nitroglycerin infusion is useful in the event of coronary ischemia or to assist in reducing preload. Epinephrine and norepinephrine infusions are also prepared in anticipation of inotropic or vasoconstrictor support. Rapid transfusion of blood and blood products introduces a significant quantity of citrate into the circulation. Large amounts of calcium chloride (up to 10 g) are used to counteract the effects of citrate on ionized calcium levels.


Relieving coronary ischemia can be directed to adjusting preload, afterload, and contractility. -Blocking drugs can slow the heart rate and reduce the force of contractility, improving myocardial oxygen delivery while reducing consumption. Nitroglycerin is useful to decrease preload, and sodium nitroprusside reduces afterload.

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Simpson JI. Eide TR. Newman SB, et al.Trimethaphan versus sodium nitroprusside for the control of proximal hypertension during thoracic aortic cross-clamping: the effects on spinal cord ischemia. Anesth Analg 1996:82:68–74.

C.8. What are the adverse effects of aortic unclamping?


Following the release of the aortic cross-clamp, a large volume of desaturated blood returns to the heart from the areas of hypoperfusion below the cross-clamp and is incompletely reoxygenated in the lungs. The transit time of a red blood cell through the pulmonary circulation is inadequate to allow hemoglobin to become fully saturated. The result is temporary systemic hypoxemia.


A dilutional coagulopathy can result from blood loss and transfusion during the repair. Even though cases have been performed in patients without the administration of blood or blood products, most TAAA repairs require homologous blood and blood product transfusion. Use of partial or complete CPB can cause significant platelet dysfunction.


A variety of metabolic and electrolyte derangements occur during the surgery. Massive transfusions are accompanied by hyperkalemia and hypocalcemia. The metabolic acidosis resulting from hypoperfusion can also lead to changes in serum potassium. Glucose regulation can be difficult because of preexisting diabetes in many of these patients, as well as the surgical stress response.


Hypoperfusion of the lower segments of the aorta, and the organs and vascular beds they supply, force a conversion from aerobic to anaerobic metabolism and production of lactate. The quantity of lactate produced during repair of a TAAA can quickly overwhelm the physiologic buffering capacity. The adverse affects seen with acute acidosis include ventricular irritability, decreased myocardial contractility, and vasodilatation. Release of the cross-clamp presents a large acid load to the lungs. As a result, a rise in PaCO2 has been noted immediately following declamping.


Declamping presents a challenge to hemodynamic management. Systemic vascular resistance and arterial blood pressure can drop by 70% to 80%. Upper extremity blood flow decreases in favor of increasing lower extremity flow. The cause of this increase in lower extremity flow is reactive hyperemia of the ischemic vascular beds. The increased capacitance of the regions below the cross-clamp is a result of reflex vasodilatation and venous pooling, and the effect of vasodilating metabolites and hypoxemia on vascular smooth muscle. In addition, ischemic metabolites have a negative inotropic effect on cardiac function, depressing contractility and lower cardiac output.

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Gelman S. The pathophysiology of aortic cross-clamping and unclamping. Anesthesiology 1995:82:1026–1057.

Gertler JP. Cambria RP. Brewster DC, et al.Coagulation changes during thoracoabdominal aneurysm repair. J Vasc Surg 1996:24:936–943.

O'Conner CJ. Rothenberg DM. Anesthetic considerations for descending thoracic aortic surgery: part II. J Cardiothorac Vasc Anesth 1995:9:734–747.

C.9. What can be done to minimize the adverse effects of aortic unclamping?

Volume administration is a pivotal component to avoiding or reducing the degree of declamping shock. Venous access and infusion equipment should be available to permit infusion rates of 0.8 to 1.5 L/minute and provide the necessary volume to offset the postclamp vasodilatation. Gradual release of the clamp by the surgeon can limit the acute nature of the drop in blood pressure and allow time for adequate volume resuscitation. Vasoconstrictors can be used to temporarily offset the hypotension. Their effect, however, is predominantly on the upper extremity vascular beds. Calcium salts can be administered to provide a brief boost in contractility to counter the myocardial depressant effects of the venous return from below the clamp.

Adequate reversal of heparin activity with protamine is the first step in correcting the coagulopathy. Platelet and fresh frozen plasma infusions correct the dilutional coagulation defects. Warming the patient reduces the likelihood of a cold-induced coagulopathy.

Increasing the FIO2, adequate suctioning of the endotracheal tube, bronchodilator therapy, positive end-expiratory pressure (PEEP), and continuous positive airway pressure (CPAP) are all essential components when faced with hypoxemia during one-lung ventilation. Hypoxemia following the release of the cross-clamp can be reversed with inflation of the left lung until the period of desaturation resulting from declamping is complete. Mannitol, through its role as a free-radical scavenger, has been shown to decrease the concentrations of thromboxane B2 and its effect on pulmonary resistance and vascular permeability.

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Gelman S. The pathophysiology of aortic cross-clamping and unclamping. Anesthesiology 1995:82:1026–1057.

Gertler JP. Cambria RP. Brewster DC, et al.Coagulation changes during thoracoabdominal aneurysm repair. J Vasc Surg 1996:24:936–943.

C.10. How would you approach the anesthetic in this case?

Induction and before cross-clamp

Induction of anesthesia begins after placement of an arterial line and a large-bore intravenous line. The induction is directed at maintaining normal blood pressure and heart rate. A combination of narcotics, benzodiazepines, and muscle relaxant is most often used. Adequate ventilation is established and a double-lumen tube, Univent, or endotracheal tube with bronchial blocker is placed. Placing a double-lumen tube can be problematic because of the anatomic relationship of the aneurysmal descending aorta to the trachea. In addition, compression of the trachea by the aneurysm can lead to tracheomalacia. Insertion of the endotracheal tube in that weakened area could cause tracheobronchial disruption or rupture of the aneurysm. Further large-bore intravenous access and central monitoring are placed following induction. A 14-gauge Touhy needle is used to introduce a large [1.5 mm internal diameter (ID)] spinal drain into the subarachnoid space at the L3 to L5 level. Placement of the drain before or following induction is a personal preference. The rapid infusion system is primed, connected to the intravenous lines, and tested to ensure adequate flow for resuscitation later in the case. The patient is positioned in the right lateral decubitus position and the preclamp infusions are begun. The bicarbonate infusion is begun at 1 mEq/kg/hour and the dopamine infusion is started at 2 g/kg/minute. Correct tube or blocker placement is confirmed and one-lung ventilation is begun during surgical prep. One-lung ventilation is instituted early to ensure that the patient can tolerate it during the surgical procedure. We allow patients' temperatures to drift down to near 33°C to protect the spinal cord. Patients are slightly hyperventilated in an attempt to reduce intracranial and spinal cord pressure. Normal blood pressure and heart rate are maintained until placement of the cross-clamp. A well-controlled heart rate decreases myocardial oxygen consumption, increases time for coronary perfusion, and decreases shear forces on the aorta. Preclamp blood pressure is kept in a range in which organ perfusion is maintained, but excessive pressure is not exerted on the walls of the aorta. Mannitol and furosemide are administered 15 to 20 minutes before clamp placement. Just before cross-clamp, vasodilator infusions are begun in anticipation of the hemodynamic changes associated with placing of the clamp. Heparin 100 units/kg is administered 5 minutes before clamp placement for systemic anticoagulation.

During cross-clamp

As mentioned previously, clamping of the proximal descending aorta results in an abrupt increase in afterload. In an attempt to decrease the acute rise in blood pressure and vascular resistance, arterial vasodilators and additional anesthetic are administered. The use of isoflurane during this period is useful as an anesthetic and vasodilator. Vasodilators are adjusted to permit systolic blood pressure to remain between 100 to 140 mm Hg. Higher blood pressure puts strain on the clamp and may cause it to slip. Blood pressure will decrease from profound reductions in preload secondary to blood loss. Using hypovolemia as a method of blood pressure control leaves the patient underresuscitated at the time of declamping. Rapid blood loss with incision into the aneurysm and collateral intercostal artery bleeding necessitates continuous volume administration. PA pressures can be used to assess volume status at this point during the surgery. After placement of the cross-clamp, the PA pressures rise acutely in response to the change in loading conditions of the left ventricle. These new PA pressures can be used as a reflection of euvolemia under these new loading conditions and in the absence of cardiac dysfunction. As the completion of the anastomosis is reached, large amounts of additional volume need to be infused into the patient. Vasodilating infusions are stopped and ventilation is slightly increased. Checking the PA pressures and TEE images should provide enough information about LV preload to gauge the volume requirement to provide stable hemodynamics immediately after declamping the aorta. Hypervolemia and systolic hypertension are short-term goals that must be achieved just before release of the cross-clamp.

Removal of clamp and postclamp

Removing the clamp leads to a state of hypovolemic shock. Infusion of blood, colloid, and crystalloid at 800 to 1,500 mL/minute may be necessary to maintain blood pressure and fill the ischemic and dilated vascular beds. In a normal left ventricle, volume will rapidly correct the transient hypotension of declamping. A bolus of calcium assists the left and right ventricles to face the negative inotropic, vasodilating, and pulmonary vasoconstricting effects of the desaturated, acidotic venous return. A ventricle with preexisting dysfunction or new ischemia will need inotropic support and volume to resolve the hypotension of declamping. Occasionally, vasoconstrictors can help support blood pressure and maintain adequate perfusion pressure until the volume and cardiac function issues are resolved. Minute ventilation is increased to compensate for the abrupt acid load presented to the lungs. Two-lung ventilation can be reinstituted if inadequate oxygenation results from the return of profoundly deoxygenated blood to the pulmonary circulation. Later in the postclamp period, anesthetic management is similar to that of a trauma patient. Establishment of normal coagulation, euvolemia, and normal metabolic and electrolyte balance are the major concerns. Calcium and potassium are affected by the administration of blood products, changes in renal function, and the use of citrate as an anticoagulant during the procedure. Acidosis from hypoperfusion continues to be an issue and can be treated with volume and bicarbonate. Coagulation is affected by the turnover and washout of the patient's blood volume. Plasma, platelets, and reversal of heparin can return coagulation to near normal levels. Warming the patient at this point becomes a challenge. After intentionally allowing body temperature to drift to 33°C, rewarming the patient becomes important because of the temperature's effect on coagulation and cardiac conduction. Warming fluids, heating fresh gas flow, and raising ambient room temperature all assist in the process. However, the volume requirements and size of the incision make this a difficult task. If a double-lumen tube was placed at the start of the case, it should be replaced with a single-lumen endotracheal tube to ease postoperative pulmonary and ventilatory care.

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O'Connor CJ. Rothenberg DM. Anesthetic considerations for descending thoracic aortic surgery: part I. J Cardiothorac Vasc Anesth 1995:9:581–588.

O'Connor CJ. Rothenberg DM. Anesthetic considerations for descending thoracic aortic surgery: part II. J Cardiothorac Vasc Anesth 1995:9:734–749.

D. Postoperative Management

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D.1. What postoperative complications can you anticipate?

Morbidity and mortality are significantly higher in the elderly population and in cases of reoperation. Postoperative complications include myocardial infarction (MI), respiratory failure, renal failure, bleeding, spinal cord injury, and cerebral vascular accidents.


The incidence of perioperative MI is 7% to 13% with a mortality rate as high as 15%.

Respiratory failure

Thoracic and abdominal incisions increase the likelihood of respiratory complications. Respiratory failure occurs in 20% of patients. Many of these patients have preexisting pulmonary disease. The traumatic sequelae of one-lung ventilation further impair ventilation. The release of vasoactive substances from ischemic lower extremities and lung hypoperfusion can lead to interstitial edema. Risk of respiratory failure increases with cardiac and renal failure, age older than 72 years, and a history of COPD or smoking.

Renal failure

The incidence of renal failure is 2.7% to 14% after repair of TAAA. A duration of cross-clamp greater than 30 minutes is the major determinant of postoperative renal dysfunction. Risk factors for postoperative dialysis are:

  • Age (older than 50)

  • CAD

  • Diabetes mellitus (DM)

  • Elevated preoperative serum creatinine

  • Transfusion of multiple blood products


The incidence of reoperation for bleeding is 3% to 5%. Causes include:

  • Heparinization

  • Thrombocytopenia

  • Hypothermia

  • Acidosis

  • Factor deficiency

  • Disseminated intravascular coagulation (DIC)

  • Hepatic failure

  • Chronic renal failure

Spinal cord injury/paraplegia

The incidence of paraplegia is 2% to 40% and depends on type of aneurysm, surgical technique, and duration of ischemia. Paraplegia is increased significantly with emergency surgery and a cross-clamp time longer than 30 minutes. The presentation of spinal cord injury related to this surgery is a loss of motor function and pinprick sensation.

Cerebrovascular accident

It is a well documented complication with a 9.6% incidence.

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Acher CW. Wynn MM. Hoch JR, et al.Cardiac function is a risk factor for paralysis in thoracoabdominal aortic replacement. J Vasc Surg 1998:27:821–830.

Cambria RP. Davison KJ. Zannetti S, et al.Thoracoabdominal aneurysm repair. perspective over a decade with the clamp-and-sew technique. Ann Surg 1997:226:294–305.

Godet G. Fleron MH. Vicaut E, et al.Risk factors for acute postoperative renal failure in thoracic or thoracoabdominal aortic surgery: a prospective study. Anesth Analg 1997:85:1227–1232.

LeMaire SA. Miller CC III. Conklin LD, et al.A new predictive model for adverse outcomes after elective thoracoabdominal aortic aneurysm repair. Ann Thorac Surg 2001:71:1233–1238.

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