Etiology

The causes of thoracic aortic aneurysms are summarized in Table 11-1. Atherosclerotic degeneration is the most common cause of aneurysms involving the descending thoracic and thoracoabdominal aorta. Risk factors include increased age, smoking, and hypertension.

Table 11-1 Causes of Thoracic Aortic Aneurysms

Cystic medial necrosis is a degenerative condition characterized by fragmentation of the elastic fibers and loss of smooth muscle within the medial layer of the aortic wall, resulting in a loss of tensile strength. Cystic medial necrosis typically affects the ascending aorta and can lead to aneurysm and dissection. The condition is more common in males than females and typically develops in people over 40 years of age. Some degree of medial degeneration of the aorta is part of the normal aging process and accounts for the age-related increase in aortic dimensions. Marfan syndrome is an autosomal-dominant connective tissue disorder characterized by defective synthesis of the glycoprotein fibrillin, predisposing to cystic medial necrosis. Patients with Marfan syndrome are at high risk for developing early-onset aneurysms and dissections of the thoracic aorta.

Aneurysms of the proximal ascending aorta may result from chronic flow turbulence due to aortic valve stenosis (poststenotic dilatation). In addition, patients with bicuspid or unicuspid aortic valves are at increased risk for aortic aneurysm formation due to primary structural abnormalities of the aortic wall.¹ Thoracic trauma, usually a sudden deceleration injury, is a rare cause of chronic aneurysm formation. This is usually caused by intimal disruption in the area of the aortic isthmus. A pseudoaneurysm (false aneurysm) is a collection of thrombus and connective tissue outside the aortic wall that occurs as a result of a contained rupture. Pseudoaneurysms typically occur secondary to infection, trauma, or previous aortic surgery.

Classification

Aneurysms of the thoracic aorta can be classified on the basis of their anatomic position. Ascending aortic aneurysms arise anywhere from the aortic valve to the innominate artery. Aortic arch aneurysms involve aorta bounded by the brachiocephalic vessels. Descending thoracic and thoracoabdominal aneurysms arise distal to the left subclavian artery. Thoracoabdominal aneurysms are further divided according to the Crawford classification (see Fig. 11-1).

Figure 11.1 The Crawford classification of thoracoabdominal aneurysms. Type I aneurysms arise distal to the left subclavian artery and extend to the level of the superior mesenteric artery but above the renal arteries. Type II aneurysms arise distal to the left subclavian and extend to below the renal arteries. Type III aneurysms arise from below the level of the sixth intercostal space and extend to below the renal arteries. Type IV aneurysms arise from the level of the twelfth intercostal space (supraceliac) and extend to below the renal arteries.

Natural History

An aortic aneurysm is a slowly progressive but intrinsically lethal condition that eventually undergoes rupture or dissection. The primary determinant of adverse outcome is aneurysm size: a patient with a maximal aortic dimension of 6 cm has an annual risk for rupture, dissection, or death of 14%.²

The growth rate of aneurysms is not linear, tending to accelerate as the aneurysm increases in size (see Wall Stress and Aneurysm Growth in Chapter 1). Aneurysms grow faster in patients who smoke, in patients who are hypertensive, in aortas with dissections, and in the thoracic aorta rather than the abdominal aorta.

Surgical intervention is recommended when the maximal aortic diameter exceeds 5.5 cm in the ascending aorta and 6 to 6.5 cm in the descending aorta.^2,3 These recommendations are based on the relative risks for rupture or dissection compared with the risks involved in surgery.

Aneurysms caused by Marfan syndrome display accelerated unpredictable growth patterns and have a tendency to rupture or dissect at a smaller size than do aneurysms in patients without Marfan syndrome. This is particularly the case if there is a family history of early complications. Surgery is recommended for patients with Marfan syndrome when the maximal diameter exceeds 5 cm in the ascending aorta and 6 cm in the descending aorta.²

Clinical Features and Investigations

Thoracic aortic aneurysms are commonly asymptomatic and are usually discovered incidentally when a chest radiograph or echocardiogram is performed for some other reason. A proportion of patients experience chest pain, which is caused by rapid expansion of the aneurysm itself or, rarely, by bony erosion. Occasionally, a large aneurysm causes symptoms that result from pressure on adjacent structures. Hoarseness may develop due to stretching of the recurrent laryngeal nerve. Pressure on the trachea and left main bronchus can cause stridor, dyspnea, atelectasis, or pneumonia. Pressure on the esophagus may cause dysphagia.

Aneurysms involving the aortic root commonly cause aortic regurgitation secondary to annular dilatation. Thus, an aortic aneurysm may be identified in a patient who presents with aortic regurgitation or congestive cardiac failure.

The aneurysm may be apparent on a chest radiograph. With an ascending aneurysm, there may be a prominent right aortic border on the frontal projection and filling in of the upper substernal space on the lateral projection. With an arch aneurysm there may be widening of the mediastinum on the frontal projection. An enlarged descending thoracic aorta may be seen behind the heart on the frontal and lateral projections (Fig. 11-2).

Figure 11.2 Chest radiograph showing a descending thoracic aortic aneurysm and the abnormal lateral border of the aneurysm (arrows).

Imaging of thoracic aortic aneurysms may be undertaken by echocardiography, computed tomography (CT), or magnetic resonance (MR) imaging. Echocardiography allows accurate assessment of aortic regurgitation, aortic leaflet morphology, and ventricular function, but it may not fully delineate the anatomic extent and relationships of the aneurysm. Echocardiography is particularly poor at imaging the distal ascending aorta and aortic arch. To image the aneurysm itself accurately, either a contrast CT scan (Fig. 11-3A) or MR imaging scan is required. For patients undergoing aneurysm surveillance, conventional axial CT scanning is sufficient. For operative planning, CT or MR imaging with three-dimensional reconstruction is extremely helpful (Fig. 11-3B).

Figure 11.3 CT scan of a descending thoracic aortic aneurysm. A, The aneurysm in transverse section. B, The aneurysm in coronal reconstruction. Eccentric mural thrombus is present (arrows). The aorta is very tortuous.

Treatment of Thoracic Aneurysms

In patients with small aneurysms, regular surveillance by CT scanning is indicated; the frequency of scanning is determined by the size and growth pattern of the aneurysm. Medical treatment primarily involves control of hypertension. β Blockers are a good choice for blood pressure control because they reduce tension in the aneurysm wall and, unlike arteriolar vasodilators, do not increase shear forces in the aorta.⁴ Drug treatment of hyperlipidemia and diabetes may also be indicated. Smoking cessation, diet, and exercise are all important preventive strategies for atherosclerosis.

Aneurysms involving the ascending aorta, aortic arch, and the thoracoabdominal aorta typically require open surgical repair. Aneurysms limited to the descending thoracic aorta may be suitable for endovascular stent grafting. Concomitant aortic valve and coronary artery bypass graft surgery may also be indicated.

Preoperative Assessment

Aortic aneurysms and dissections typically occur in older patients with histories of smoking, hypertension, and chronic obstructive pulmonary disease. There is frequently coexisting coronary artery, carotid artery, and peripheral vascular disease. Furthermore, open repair of thoracic aortic aneurysms imposes a huge physiologic insult on patients. Thus, it is essential to fully investigate and optimize patients prior to surgery.

An echocardiogram should be performed on all patients; with particular emphasis on aortic valve and ventricular function. Patients over 40 years of age and those with risk factors for coronary artery disease should undergo coronary angiography.⁵

More than one third of patients undergoing surgery for thoracic aortic aneurysms have either a diagnosis of chronic obstructive pulmonary disease or a history of heavy smoking.⁶ These patients should have spirometry and arterial blood gases performed preoperatively. They are also likely to benefit from a period of smoking cessation, chest physiotherapy, and appropriate treatment of the infective and bronchospastic components of their respiratory diseases. The management of patients with obesity, renal failure, carotid disease, and diabetes is similar to that outlined in Chapter 9.

Etiology

The causes of aortic dissection are similar to the causes of aortic aneurysm (see Table 11-1). Indeed, dissection, intramural hematoma, and atherosclerotic plaque rupture can all complicate an aortic aneurysm. An additional cause of aortic dissection is iatrogenic aortic injury due to surgical manipulations such as the placement of aortic cannulas during cardiopulmonary bypass.

Classification

Most aortic dissections begin in the ascending aorta and extend distally, although between 5% and 10% begin in the arch, and 30% to 35% begin in the first part of the descending aorta. There are two main classification systems, based on the extent of aortic involvement (Fig. 11-4). The Stanford classification is used here.⁹

Figure 11.4 The Stanford classification of aortic dissections. Type A dissections involve the ascending aorta; they may be limited to the ascending aorta (1) or extend into the descending thoracic aorta (2). Type B dissections involve the descending thoracic aorta (3). A dissection that involves only the aortic arch is not classified by the Stanford system, but if it subsequently extends proximally into the ascending aorta, it becomes type A.

Rights were not granted to include this figure in electronic media. Please refer to the printed book.

(From Daily PO, Trueblood HW, Stinson EB: Management of acute aortic dissections. Ann Thorac Surg 10:237-247, 1970.)

Clinical Features and Investigations

Acute aortic dissection (type A and B) classically presents with the abrupt onset of excruciating chest pain that is commonly described as having a tearing quality. Anterior chest pain is more likely with type A dissection; back pain is more common with type B dissection. However, there is wide variation in presenting symptoms, and aortic dissection should be considered in all patients who present with acute severe chest pain.

Type A Dissection

Type A aortic dissections can result in the following complications:

• Pericardial tamponade and sudden death due to rupture of the aorta into the pericardium

• Aortic regurgitation due to extension of the dissection into the aortic root.

• Myocardial ischemia or infarction due to obstruction of the orifice or avulsion of the right coronary artery. (The left coronary is rarely involved.)

• Obstruction of a major branch artery, causing hypoperfusion of the brain, spinal cord, kidneys, or gastrointestinal tract.

• Free rupture into the thoracic cavity. This is usuallyrapidly fatal.

Patients commonly present with shock due to the combined effects of pericardial tamponade and aortic regurgitation. In the absence of these complications, patients may be hypertensive. Patients may develop a major neurologic deficit, such as impaired consciousness, hemiplegia, paresthesia, or paraplegia. Pulses (brachial, carotid, femoral) may be weak, absent, or asymmetric. Four-limb blood pressure measurements may show marked variability. The chest radiograph may demonstrate widened mediastinum and loss of the aortic knuckle (Fig. 11-5).

Figure 11.5 Chest radiograph showing a widened mediastinum (arrows) caused by type A dissection.

Imaging

Patients who present with symptoms and signs consistent with aortic dissection require urgent diagnostic imaging. Options include transesophageal echocardiography (TEE), CT scanning, MR imaging, and aortography, all of which have a sensitivity and specificity greater than 90%.¹⁰ Intramural hematoma may be difficult to diagnose with any of these techniques. The preferred initial investigation varies according to the institution, but CT scanning is the most widely used modality.¹¹ CT scanning has the advantage of being rapid (unlike MR imaging) and does not require sedation or general anesthesia (unlike TEE). Aortography is rarely indicated other than as part of a stenting procedure. CT scanning demonstrates the extent of the dissection (Fig. 11-6) and the presence of any pericardial blood but does not usually demonstrate the entry tears or any associated aortic regurgitation.

Figure 11.6 CT scan showing a type A dissection. A, In the transverse section, the intimal flap (arrows) is seen in the ascending and descending aorta. B, In the sagittal reconstruction, the false lumen (arrows) is seen immediately distal to the aortic arch and also within the abdomen.

TEE is the most useful investigation for determining the severity of any associated aortic regurgitation (Fig. 11-7) and may provide information on the site of the entry tears. TEE is also useful for identifying pericardial effusions and myocardial ischemia. The administration of intravenous sedation for TEE in a patient with suspected dissection is hazardous because it may precipitate either hypotension (due to the effects of sedative drugs in a patient with pericardial tamponade) or hypertension (due to patient anxiety).

Figure 11.7 Transesophageal echocardiography of type A dissection. A, The intimal flap (arrow) in the proximal ascending aorta. A pericardial fluid collection (P) can also be seen. B, A broad jet of aortic regurgitation (arrow).

If the diagnosis of dissection is confirmed by CT scanning, TEE examination of the aortic valve is best performed under general anesthesia in the operating room. If the diagnosis is not confirmed by CT scanning but there is a high index of suspicion for dissection, then further imaging is required. In a stable patient MR imaging may be used. Alternatively, in an unstable patient, TEE may be performed in the operating room under general anesthesia and with the surgical team on standby.

Management

Postoperative Care Following Endovascular Stent Grafting

After uncomplicated endovascular stent graft repair, patients are typically awakened from anesthesia and transferred to a high-dependency environment for 12 to 24 hours of monitoring. Slight to moderate back pain and transient postimplantation syndrome, with low-grade fever, leukocytosis, and raised C-reactive protein are common.¹⁸

A number of serious early and late complications have been reported following endovascular stent grafting (Table 11-2). Postoperative renal failure may develop for a number of reasons, including preexisting renal dysfunction, exposure to radiographic contrast agents, intraoperative hemodynamic instability and, rarely, stent occlusion of a renal artery. Urine output should be measured hourly for 24 hours postoperatively. In patients with preexisting renal impairment, the administration of N-acetylcysteine prior to the procedure should be considered (Chapter 33).

Table 11-2 Complications of Endovascular Aortic Stent Grafting

Modified from Gowda RM, Misra D, Tranbaugh RF et al: Endovascular stent grafting of descending thoracic aortic aneurysms. Chest 124:714-719, 2000.

Bowel or hepatic ischemia may occur due to the stent’s occlusion of the arterial blood supply or an embolus involving the celiac trunk or superior mesenteric artery. The gradual onset of severe abdominal pain in the absence of signs of peritonism indicates the need for urgent abdominal imaging by CT or MR imaging scan to exclude mesenteric vascular insufficiency. Once signs of peritonism, acidosis, and shock have developed, bowel infarction is likely to have already developed.

Spinal cord ischemia is rare but can occur. In one small series, 3 of 53 patients undergoing endovascular stent grafting of the descending thoracic aorta developed spinal cord ischemia and 2 of them were irreversibly paralyzed.²⁴ The onset of neurologic signs commonly occurs hours or days after the procedure.^24,25 Previous or concomitant abdominal aortic aneurysm repair and the use of long or multiple stent grafts that extend into the T8 through L2 region increase the risk for paraplegia.^15,26 In patients at high risk for paraplegia, cerebrospinal (CSF) fluid drainage (see subsequent material) should be considered prior to the procedure or as a rescue maneuver if symptoms develop postoperatively.^24,26,27

A complication that is specific to endovascular stent grafting is endoleak, in which there is persisting flow into the aneurysm or the false lumen of a dissection. Endoleaks may occur at the proximal or distal attachment site (type I), in a retrograde manner via side branches (type II), or through defects in the graft itself (type III). Leaks at the junction of two sequential grafts can also occur. An endoleak may be diagnosed at the time of stent deployment or during the early or late postoperative period. Endoleak may cause pain due to expansion of the aneurysm or dissection, but in many cases symptoms are minimal and the problem is identified on CT scanning at the time of stent deployment or at routine follow-up (Fig. 11-9). If an endoleak is identified it may be left and followed up with serial CT scans or a repair may be attempted. For type I endoleak, molding the stents by using a balloon catheter or deploying additional stents may be undertaken; for a type II endoleak, angiographic coiling of feeder vessels may be performed. Aneurysm expansion is an indication to intervene for an endoleak.

Figure 11.9 Computed tomography scan showing a type 1 endoleak. Intravenous contrast (arrow) can be seen outside the endovascular stent in the descending thoracic aorta. Hematoma can be seen encircling the stent. A stent is also present in the ascending aorta.

Following endovascular stent grafting, ongoing surveillance of the aorta should be undertaken (usually by contrast CT scanning with three-dimensional reconstructions) to look for evidence of stent migration, endoleak, or increase in size of the lesion. CT scans should be obtained at discharge, every 3 to 6 months for the first 1 to 2 years, and then yearly thereafter.

Ascending Aorta and Aortic Arch

For aortic syndromes involving the ascending aorta and aortic arch, open repair is typically performed through a midline sternotomy with the use of cardiopulmonary bypass (CPB). Modifications to the CPB technique described in Chapter 9 may be required. In the presence of aneurysm or dissection, it may not be possible to position the arterial bypass cannula in the proximal ascending aorta, in which case the distal ascending aorta, right axillary artery, or femoral artery is used.

For a type A dissection it is necessary to replace only that part of the aorta that contains the entry tears, not the entire length of the dissection. If an aneurysm or the entry tear of a type A dissection extends into the aortic arch, it is not possible to place a cross-clamp above the pathology without compromising blood supply to the brain. In this situation, surgical repair of the aortic arch is performed using hypothermic circulatory arrest. On CPB, the patient is cooled to a state of deep hypothermia (<20°C), the heart-lung machine is turned off, and the patient is exsanguinated into the venous reservoir. Circulatory arrest provides a bloodless surgical field that is not obstructed by clamps and cannulas. The main danger in hypothermic circulatory arrest is neurologic injury, the incidence of which depends on many factors, but primarily on the duration of circulatory arrest and the patient’s age.^28,29 Although there is no absolutely safe period of circulatory arrest, the incidence of neurologic injury increases substantially beyond 30 minutes at a temperature of 20°C.²⁸ In an attempt to reduce the incidence of neurologic injury, techniques of selective cerebral perfusion have been developed, in which cold, oxygenated blood is perfused (usually) antegrade via the carotid arteries during the period of circulatory arrest. One technique for antegrade cerebral perfusion, which relies on an intact circle of Willis, involves placing the arterial bypass cannula in the right axillary artery. During circulatory arrest, blood is perfused down the arterial cannula at low flow rates (10 ml/kg/min) with the innominate artery clamped, thus directing flow up the right common carotid artery. Excellent neurologic outcome has been achieved with this technique.³⁰ If selective cerebral perfusion is used, some surgeons limit systemic cooling to 20° to 25°C.

Descending Thoracic Aorta

For surgical procedures involving the descending thoracic aorta, repair is performed through a left thoracotomy, utilizing one-lung ventilation via a double-lumen endotracheal tube.

A number of surgical strategies are used. The most simple is the “clamp-and-sew” technique, in which the proximal thoracic aorta is cross-clamped and the distal aorta repaired (Fig. 11-10A). Some surgeons have achieved good results with this approach.³¹ However, cross-clamping the descending thoracic aorta in the absence of CPB or distal aortic perfusion is associated with a number of adverse hemodynamic and metabolic effects. Proximal to the clamp (the heart and the head) there is marked hypertension, increased left ventricular afterload, and the potential for myocardial ischemia. Distal to the clamp (the abdominal organs and spinal cord) there is end-organ hypoperfusion with the potential for paraplegia, mesenteric ischemia, and renal failure. Unclamping may be associated with profound hypotension and acidosis. Outcomes of the clamp-and-sew technique are critically dependent on the aortic cross-clamp time.

Figure 11.10 Repair techniques for aneurysms involving the descending thoracic aorta. See text for details.

Three techniques that are used to decompress the proximal aorta and maintain perfusion to the distal aorta during aortic cross clamping are (1) passive aortoaortic shunting across the clamped area using a Gott shunt; (2) left heart (atriofemoral) bypass; and (3) partial (femoral-femoral) bypass. With left heart bypass (see Fig. 11-10B), oxygenated blood is drained from the left atrium and is returned to the femoral artery. A simple heparin bonded circuit consisting of a heat exchanger and a constrained vortex pump is typically used. Full heparinization is not required. With partial bypass (see Fig. 11-10C), deoxygenated blood is drained from the femoral vein, passes through a heat exchanger and a membrane oxygenator, and is returned to the femoral artery. Both techniques require ventilation and normal cardiac function throughout the period of bypass support. The use of a heat exchanger in the circuits allows the use of modest hypothermia (30° to 34°C), potentially providing some neurologic protection. Distal aortic perfusion with left heart or partial bypass stabilizes hemodynamics, minimizes acidosis, and maintains perfusion to the abdominal organs but has not unequivocally been shown to reduce the incidence of paraplegia. Techniques that involve aortic cross-clamping are often combined with lumbar cerebrospinal fluid (CSF) drainage (see subsequent material). CSF drainage reduces CSF pressure and therefore helps to maintain spinal cord perfusion pressure during aortic cross-clamping. Two recent metaanalyses have demonstrated a reduction in adverse neurologic events with CSF drainage compared to without drainage.^32,33

An alternative strategy for the repair of aneurysms of the descending thoracic and thoracoabdominal aorta is the use of full CPB and hypothermic circulatory arrest. CPB is initiated with bypass cannulas placed in the femoral artery and vein, and the patient is cooled to 15° to 18°C. The proximal aortic anastomosis is completed under circulatory arrest and a second arterial cannula is placed proximally in the graft. The aorta is then repaired by means of sequential repositioning of two aortic cross-clamps, while maintaining perfusion to the upper and lower body via the two arterial cannulas. This technique is associated with an acceptable mortality rate and a low incidence of paralysis, stroke, and visceral end-organ dysfunction, particularly renal failure.³⁴

Postoperative Care Following Open Aortic Repair

Postoperative complications following open surgical repair of thoracic pathology are determined by the site of the surgery, the nature and extent of the operation, and the patient’s comorbid state. The mortality rate in patients undergoing surgery on the thoracic aorta is about 10%³⁵ but increases to more than 30% in emergency surgery.³⁶

Open repair of thoracic aortic syndromes imposes a huge physiologic insult on the patient. Surgery and CPB are often prolonged and commonly involve the use of hypothermic circulatory arrest. Myocardial dysfunction, hemodynamic instability, coagulopathy, excessive bleeding, and multiple organ dysfunction syndrome are common postoperative sequelae. However, the most feared complications are neurologic: permanent brain or spinal cord injury.

Cardiovascular Function

Both high and low cardiac-output states are seen following aortic surgery. High cardiac output may occur due to the development of the systemic inflammatory response syndrome. Low cardiac output may occur for several reasons. Postoperative myocardial stunning is common as the result of the effects of prolonged hypothermic CPB and difficulties with myocardial protection (see Chapter 9). Patients with thoracic aortic disease often have left ventricular hypertrophy and aortic regurgitation, both of which can create problems with myocardial protection. Rarely, myocardial ischemia can arise due to anatomic problems related to reimplantation of the coronary arteries following aortic root replacement (see Chapter 10). Right ventricular dysfunction may occur due to gas emboli in the anteriorly placed right coronary artery (usually with transient effects). Pericardial tamponade is not uncommon following aortic root surgery, particularly when there is marked coagulopathy.

Because of the high incidence and multiple causes of hemodynamic instability in this group of patients, routine use of a pulmonary artery catheter and early use of echocardiography is appropriate. An intraaortic balloon pump is contraindicated after surgery on the descending thoracic aorta.

Hypertension exacerbates bleeding and has the potential to cause dehiscence of aortic suture lines, with catastrophic results. Many surgeons favor keeping the blood pressure below set limits for the first few hours after aortic surgery (e.g., systolic blood pressure <110 mmHg). However, patients with aortic disease typically have preexisting severe hypertension. Thus, prolonged hypotension during the postoperative period exacerbates end-organ dysfunction, particularly of the brain, spinal cord, gut, and kidneys. However, in the longer term, effective management of hypertension is essential.

Respiratory Function

Respiratory failure is common following thoracoabdominal aortic surgery and is associated with a high mortality rate.⁶ Severe contusion of the left lung is common following procedures on the descending thoracic aorta because of the effects of surgical handling, pulmonary collapse during one-lung ventilation, and heparinization. Postoperatively the chest radiograph may demonstrate a white-out appearance that persists for some days. Lung compliance and gas exchange are often impaired and patients may require prolonged mechanical ventilation. During the initial postoperative period there may be considerable bleeding into the tracheobronchial tree from the left lung. If, at the end of surgery, endobronchial bleeding is a significant problem, the double-lumen tube may be left in place for 24 hours to protect the right lung from being soiled by blood.

Because of the effects of CPB and massive fluid shifts, it is not uncommon for there to be extensive soft tissue swelling of the face and upper airway in the immediate postoperative period. In this situation, changing the double-lumen tube for a standard endotracheal tube carries the risk of losing control of the airway, with potentially catastrophic results. The patient should be nursed in a 30-degree head-up position to help reduce facial and airway swelling.

Bleeding

Aortic surgery involves extensive suture lines that are exposed to systemic arterial pressure. Surgery is typically prolonged and commonly involves the use of hypothermia and circulatory arrest. Thus, patients are at high risk for both surgical and nonsurgical bleeding during the early postoperative period. Thrombocytopenia, coagulopathy, and fibrinolysis may require aggressive treatment. Blood component therapy should be guided by coagulation tests and thromboelastography (see Fig. 17-1). Warming a patient also helps to control bleeding, but hyperthermia should be avoided (see subsequent material).

Renal Failure

Postoperative renal impairment is common. In one large series of patients undergoing thoracoabdominal aortic operations, renal impairment (serum creatinine >3 mg/dl or 0.26 mmol/l) occurred in 18% of patients, with dialysis being required in 9% of cases.³⁷

For patients with aortic dissection (type A or type B), renal failure may occur as the result of the mechanical interruption of renal blood flow. Failure to control entry tears at the time of surgery may allow expansion of the false lumen, which carries the potential of obstructing renal, gastrointestinal, and lower-limb blood flow. Conversely, if a renal artery is supplied by a false lumen, interruption of renal blood flow may occur following surgical exclusion of the entry tear. Thus, renal failure that develops in patients with aortic dissection should not be assumed to be related to the effects of prolonged surgery and CPB. A review of the preoperative CT or MR imaging scans may suggest the possibility of a mechanical obstruction to renal blood flow, which may be confirmed by a repeat contrast CT scan. If a physical obstruction to flow is present, further intervention, such as aortic stent closure of an entry tear or fenestration of the dissection flap, may be required.

Mesenteric Ischemia

Mesenteric ischemia may occur in any patient following aortic surgery, but it is a particular problem after resection of thoracoabdominal aneurysms and after dissections (type A or B) involving the descending thoracic aorta. In patients with aortic dissection, mesenteric ischemia can occur due to mechanical obstruction of arterial flow, as described earlier. Unfortunately, by the time clinical signs develop, irreversible mesenteric infarction may have developed. Extensive infarction is virtually always fatal. Clinicians must maintain a high index of suspicion for this problem and be prepared to intervene early with further imaging or laparotomy.

Brain Injury

Permanent brain injury (focal or global deficit) occurs in up to 10% of patients following thoracic aortic surgery that involves hypothermic circulatory arrest;²⁹ increased age and the duration of circulatory arrest are the two main risk factors. The presence of extensive aortic atheroma, even of the descending aorta, is associated with an increased risk for embolic stroke.

Hyperthermia exacerbates neurologic injury and should be avoided in all patients after cardiac surgery but particularly in patients at high risk for brain or spinal cord injury. Following arrival in the ICU, patients should be rewarmed slowly and incompletely (to 36°C). For patients at very high risk for brain injury (e.g., following a prolonged period of circulatory arrest), 12 to 24 hours of deliberate postoperative hypothermia (<34°C) may be considered. The risk for neurologic injury must be weighed against the increased risk for bleeding associated with hypothermia. Neurologic outcome may also be improved by control of the blood glucose level (see Chapter 36).

Spinal Cord Ischemia

The incidence of lower-limb neurologic deficits following surgery on descending thoracic aortic aneurysms (Crawford type I or II) is as high as 30%.³² Some of these deficits are minor and the patient might recover, but the risk for permanent paralysis is a very real concern. Paraplegia or paraparesis typically presents as an anterior spinal artery syndrome, including loss of motor function and pinprick sensation but preservation of vibration and position sense.

As noted earlier, lumbar CSF drainage appears to reduce the risk for paralysis and may also reverse any new-onset paralysis that develops during the postoperative period.³⁸ CSF drains are normally inserted at the L3/4 or L4/5 disk spaces. Some anesthesiologists prefer to insert the catheters the night before surgery to allow time for any epidural bleeding to settle. CSF drainage should continue for at least 24 hours following surgery, aiming to keep the CSF pressure less than 10 to 12 mmHg. If there are no signs of paralysis, the catheter can be capped at 24 hours and the patient observed for a further 24 hours before the catheter is removed. If there are signs of lower-limb weakness, the CSF should be drained to a lower target pressure in an attempt to reverse the weakness. If there is evidence of paralysis but CSF drainage has not been performed, the insertion of a catheter and drainage of CSF should be considered. Spinal cord perfusion pressure is also dependent on systemic arterial blood pressure; therefore hypotension should be avoided. If possible, patients should be awakened early so their neurologic status can be assessed.

The incidence of serious side effects with lumbar CSF drainage is low—less than 1%.^32,39 The most important side effects are meningitis and hematoma (subdural or epidural). While the catheter is in situ, daily samples of the CSF should be sent for microbiologic culture. If meningitis is suspected, the catheter should be removed and antibiotic therapy started. Staphylococcus aureus is the most likely infective pathogen. It is prudent to avoid removing the catheter while the patient is coagulopathic or if the CSF is heavily blood stained.

Analgesia

Extensive left thoracotomy for descending thoracic or thoracoabdominal aortic pathology is associated with severe pain that can contribute to postoperative respiratory insufficiency and myocardial ischemia. Excellent analgesia can be obtained with a thoracic epidural analgesia, but this technique can potentially mask the signs of paraplegia. If epidural analgesia is used, the catheter should be inserted prior to surgery while the patient is awake and hemostasis is normal. Provision of analgesia by means of an epidural opioid (see Chapter 12) instead of a local anesthetic facilitates neurologic assessment. Alternatives to epidural analgesia include a paravertebral block and intravenous opioids. Once the patient is awake, intravenous opioids may be administered by a patient-controlled analgesia system.