Thoracic aortic diseases are generally surgical problems and require surgical treatment (Table 17-1). Acute aortic dissections, rupturing aortic aneurysms, and traumatic aortic injuries are surgical emergencies. Subacute aortic dissection and expanding aortic aneurysms require urgent surgical intervention. Stable thoracic or thoracoabdominal aortic aneurysms (TAAAs), aortic coarctation, or atheromatous disease causing embolization may be considered for elective surgical repair. Increased public awareness of thoracic aortic disease, early recognition of acute aortic syndromes by emergency medical personnel, improved diagnostic imaging technology for the diagnosis of thoracic aortic disease, and an aging population all contribute to the increased number of patients requiring aortic surgery. Furthermore, improvements in the surgical treatment of thoracic aortic diseases combined with increased treatment options such as endovascular stent repair have led to an increased number of patient referrals to centers specializing in the management of patients with thoracic aortic diseases. Improved treatment and survival after aortic surgical procedures often provide a cure for the original disease but have created new and unique problems. An increasing number of patients who have had prior aortic surgical procedures require reoperation for long-term complications of aortic surgery such as bioprosthetic valve or graft failure, aortic pseudoaneurysm at old vascular graft anastomosis, endocarditis, or progression of the original disease process into native segments of the thoracic aorta.

Table 17-1 Diseases of the Thoracic Aorta That Are Amenableto Surgical Treatment

Adapted from Kouchoukos NT, Dougenis D: Surgery of the aorta. N Engl J Med 336:1876, 1997.

The anesthetic management of surgical patients requiring aortic surgery presents some distinctive medical problems in addition to the usual considerations associated with major thoracic or thoracoabdominal operations. The process of repairing or replacing a portion of the thoracic aorta usually requires the temporary interruption of blood flow, creating the potential for ischemia or infarction of almost any major organ system in the body. Strategies to provide organ perfusion, to protect organs from the consequences of hypoperfusion, and to monitor and treat end-organ ischemia during aortic operations are critical aspects of the anesthetic management for thoracic aortic diseases and contribute importantly to the overall success of operations. Some of the procedures performed and managed by surgeons and anesthesiologists for organ protection during thoracic aortic operations, such as partial left-sided heart bypass for distal aortic perfusion, deep hypothermic circulatory arrest (DHCA), selective antegrade or retrograde cerebral perfusion (ACP or RCP), and lumbar cerebrospinal fluid (CSF) drainage, are practiced routinely in no other area of medicine.

GENERAL CONSIDERATIONS FOR THE PERIOPERATIVE CARE OF AORTIC SURGICAL PATIENTS

Patients undergoing thoracic aortic operations of any type share common considerations for the safe conduct of anesthesia and perioperative care (Table 17-2).

Table 17-2 General Considerations for the Anesthetic Care of Thoracic Aortic Surgical Patients

Preanesthetic Assessment

Urgency of the operation (emergent, urgent, or elective)

Pathology and anatomic extent of the disease

Median sternotomy vs. thoracotomy vs. endovascular approach

Mediastinal mass effect

Airway compression or deviation

Preexisting or Associated Medical Conditions

Aortic valve disease

Cardiac tamponade

Coronary artery stenosis

Cardiomyopathy

Cerebrovascular disease

Pulmonary disease

Renal insufficiency

Esophageal disease (contraindications to TEE)

Coagulopathy

Prior aortic operations

Preoperative Medications

Warfarin (Coumadin)

Antiplatelet therapy

Antihypertensive therapy

Anesthetic Management

Hemodynamic monitoring

Proximal aortic pressure

Distal aortic pressure

Central venous pressure

Pulmonary artery pressure and cardiac output

Transesophageal echocardiography

Neurophysiologic monitoring

Electroencephalography (EEG)

Somatosensory evoked potentials (SSEPs)

Motor evoked potentials (MEPs)

Jugular venous oxygen saturation

Lumbar cerebrospinal fluid pressure

Body temperature

Single-lung ventilation for thoracotomy

Double-lumen endobronchial tube

Endobronchial blocker

Potential for bleeding

Large-bore intravenous access

Blood product availability

Antifibrinolytic therapy

Antibiotic prophylaxis

Postoperative Care Considerations and Complications

Hypothermia

Hypotension

Hypertension

Bleeding

Spinal cord ischemia

Stroke

Renal insufficiency

Respiratory insufficiency

Phrenic nerve injury

Diaphragmatic dysfunction

Recurrent laryngeal nerve injury

Pain management

Preanesthetic Assessment

It is important to determine the operative diagnosis because both the anesthetic management and surgical approach are dictated by the anatomic extent of the lesion and the physiologic consequences of the disease. Diseases involving the aortic root, ascending aorta, and proximal aortic arch are generally approached through a median sternotomy, whereas diseases of the distal aortic arch or descending thoracic aorta are approached through a left thoracotomy or thoracoabdominal incision. Sometimes, the operative diagnosis can be established in advance. Other times, a presumptive diagnosis has been made based on patient symptoms or available reports and the definitive diagnosis needs to be verified after patient arrival into the operating room by direct review of the diagnostic studies or by intraoperative transesophageal echocardiography. In either case it is important to discuss the anesthetic and operative plan with the surgical team to be properly prepared for all possible contingencies. Direct review of the actual diagnostic imaging studies such as the angiogram, computed tomographic scan, magnetic resonance image, or echocardiogram not only verifies the operative diagnosis but also provides important information that determines the surgical options. Knowing the size and anatomic extent of aortic pathology provides information about the physiologic impact and consequences of the lesion, permitting the anesthesiologist to anticipate potential difficulties associated with anesthetic procedures, problems related to the surgical repair, and postoperative complications.

Anesthetic Management

Considered as a group, any operative procedure involving the aorta from endovascular stent repairs to open repair of TAAAs is associated with the potential for catastrophic bleeding and cardiovascular collapse. For this reason, continuous diagnostic ECG monitoring, intra-arterial blood pressure monitoring, large-bore vascular access for rapid volume expansion, and ensuring the immediate availability of packed red blood cells can be justified in virtually every patient. Central venous access for monitoring the right atrial pressure and the administration of vasoactive drug therapy to control the circulation can also be justified in almost all cases. Pulmonary artery catheterization to measure pulmonary artery pressures, cardiac output, and mixed venous oxygen saturation is useful for operations involving cardiopulmonary bypass (CPB), DHCA, partial left-sided heart bypass, or cross-clamping of the thoracic aorta. Routine availability and use of intraoperative TEE provide both diagnostic information and the ability to assess ventricular function.

Arguments can be made for using either the left or right radial artery for intra-arterial blood pressure monitoring. A right radial arterial catheter can detect partial occlusion or obstruction of flow into the innominate artery caused by inadvertent placement of the aortic cross-clamp too near to the origin of the innominate artery during the course of operations involving the ascending aorta or aortic arch. A right radial arterial catheter also permits monitoring of blood pressure during repair of the proximal thoracic aorta or distal aortic arch if the left subclavian artery has to be clamped. A left radial arterial catheter must be used for selective ACP via the right axillary artery. Sometimes bilateral radial arterial catheters are necessary. A femoral arterial catheter is necessary to monitor distal aortic pressure when partial left-sided heart bypass is used to provide distal aortic perfusion.

Large-bore peripheral intravenous catheters that are 16 gauge or larger provide satisfactory sites for rapid intravascular volume expansion. An intravenous administration set integrated with a fluid warming unit is desirable, particularly for the rapid administration of blood products. Often, patients coming to the operating room from other areas of the hospital already have established intravascular access with small-bore intravenous catheters at the site of large veins. One approach in this scenario is to exchange the small-bore catheter with a commercially available 7.5- to 8.5-Fr large-bore rapid infusion catheter over a sterile guidewire. The only precaution in the use of these catheters is to ensure that the vein is large enough to accept the larger-diameter catheter. Alternatively, a large-bore central venous catheter, usually an 8.5-Fr introducer sheath, 9-Fr introducer/multiple-access catheter, or hemodialysis catheter, placed in the internal jugular, subclavian, or femoral vein can be used for volume expansion. When a pulmonary artery catheter is necessary, a second introducer sheath for volume expansion can be placed also into the right internal jugular vein. For this procedure, both guidewires should be placed with at least 2 cm of separation between them. Central venous cannulation can be achieved by either anatomic landmark guidance or ultrasound guidance. Ultrasound guidance may increase both the speed and safety of venous cannulation, which is particularly advantageous in emergency operations or when the patient is hemodynamically unstable. A urinary catheter with a temperature probe to measure core temperature, together with a nasopharyngeal temperature probe, is necessary to monitor both the absolute temperature and rate of change of body temperature during deliberate hypothermia and subsequent rewarming. The temperature probe of the pulmonary artery catheter can provide core temperature monitoring, and a rectal temperature probe can be used to monitor shell temperature.

The hemodynamic condition of the patient should be reassessed immediately before the induction of general anesthesia. The decrease in arterial pressure in response to anesthetic drugs and subsequent increase in response to tracheal intubation should be anticipated. Both vasopressor drugs and vasodilator drugs should be immediately available to provide precise control of the blood pressure. Intravenous vasodilator drugs being infused to treat preoperative hypertension often need to be reduced in dose or discontinued on induction of general anesthesia. Etomidate is a useful induction agent for patients in cardiogenic shock because it does not attenuate sympathetic nervous system responses and has no direct actions on myocardial contractility or vascular tone. In hemodynamically unstable patients, a narcotic such as fentanyl in combination with a benzodiazepine such as midazolam can be subsequently titrated incrementally to maintain general anesthesia after induction with etomidate. In elective cases, general anesthesia can be induced with routine intravenous hypnotic drugs followed by a narcotic to attenuate the hypertensive responses to tracheal intubation and skin incision. Antibiotic prophylaxis administration should optimally be completed at least 30 minutes before skin incision to achieve adequate bactericidal levels in tissue. Antifibrinolytic therapy, if used, should be administered before full anticoagulation for extracorporeal circulation.

The maintenance of general anesthesia can usually be accomplished with a combination of narcotic analgesics, benzodiazepine sedative hypnotics, an inhaled general anesthetic, and a nondepolarizing muscle relaxant. Anesthetics can be reduced in response to moderate hypothermia in the range of 30°C and then discontinued during deep hypothermia at 18°C and resumed on rewarming. When electroencephalographic (EEG) or somatosensory evoked potential (SSEP) monitoring is required during surgery, barbiturates or bolus doses of propofol are avoided and the dose of the inhaled anesthetic is reduced to 0.5 MAC and kept constant to prevent anesthetic-induced changes in the monitored signals. Propofol, narcotics, and neuromuscular blocking drugs can be used during SSEP monitoring. When intraoperative motor evoked potential (MEP) monitoring is required, total intravenous anesthesia with propofol in combination with remifentanil or similar narcotic without neuromuscular blockade is necessary to ensure consistent reproducible recordings and a good-quality signal. In the majority of cases, the duration of general anesthesia is designed to persist for 1 to 2 hours after patient transfer to the intensive care unit (ICU) to permit a gradual and controlled emergence from general anesthesia. If epidural analgesia is used intraoperatively, a dilute solution of local anesthetic and narcotic is preferred to prevent hypotension caused by sympathetic nervous system blockade and to prevent complete motor or sensory blockade to permit neurologic assessment of lower extremity function.¹

The potential for blood loss and bleeding is always a consideration in operations on the thoracic aorta. The presence of intrinsic disease of the vessel wall, construction of numerous vascular anastomoses in large conducting vessels, need for extracorporeal circulation, and application of deliberate hypothermia all combine to create a situation in which blood loss and transfusion therapy are commonplace. Because blood loss can occur rapidly and unpredictably and be difficult to control, it is often prudent to have fresh frozen plasma and platelets available to provide ongoing replacement of coagulation factors during transfusion of packed red blood cells. The time delay required for laboratory testing to verify the depletion of platelets and clotting factors in the setting of ongoing blood loss is often too long to be useful as a guide for transfusion therapy. Strategies to decrease the risk of bleeding and to conserve blood include discontinuation of anticoagulation and antiplatelet therapy before surgery, antifibrinolytic therapy, the routine use of intraoperative cell salvage, biologic glue, and precise control of arterial pressure and prevention of hypertensive episodes in the perioperative period. The antifibrinolytic agents, ε-aminocaproic acid or tranexamic acid, have been safely used in the setting of thoracic aortic surgery with DHCA. The infusion of an antifibrinolytic agent should be discontinued during the period of DHCA and resumed on reperfusion. Recombinant activated factor VIIa is a synthetic hemostatic agent that promotes hemostasis by binding with tissue factor at the site of tissue injury to promote clot formation. Although experience with this agent has been limited, dramatic responses to this drug have been observed in response to coagulopathic bleeding refractory to conventional therapy in the setting of trauma, cardiac, and aortic surgery.² In the surgical setting, recombinant activated factor VIIa has been administered intravenously in doses up to 90 μg/kg and repeated once after 2 hours. Recombinant activated factor VIIa has an estimated plasma half-life of 2.6 hours and causes a rapid decrease in the prothrombin time.

Postoperative Care

After completion of the operation, the patient should be transported directly from the operating room into the ICU or postanesthetic care unit for recovery. Transfer of information to the critical care team in advance of receiving the patient is necessary to ensure an uninterrupted transition of care. Immediate application of forced-air warming prevents further temperature drift and restores normothermia even in the moderately hypothermic patient. In the absence of complications and when the medical condition of the patient is stable, the patient can be allowed to emerge from the effects of general anesthesia. Early emergence from general anesthesia is preferable because it permits early postoperative assessment of neurologic function. If the physiologic condition of the patient does not permit safe emergence from general anesthesia, sedation and analgesia can be provided in combination with mechanical ventilatory or circulatory support until the condition of the patient improves.

Common early complications include hypothermia, bleeding, hypertension, hypotension, ischemia, embolism, stroke, agitation and confusion, respiratory failure, and renal failure. Hyperglycemia, anemia, coagulopathy, electrolyte disturbances, and acid-base abnormalities are also common. Frequent hemodynamic assessment is important to control the circulation with short-acting vasoactive drug therapy and to detect cardiac arrhythmias. Arterial blood gas analysis and respiratory assessment are necessary to adjust the level of mechanical ventilatory support and determine the optimal time for safe extubation of the trachea. Laboratory testing to measure electrolyte concentration, hematologic parameters, and coagulation profile is necessary to institute immediate corrective measures. Maintaining glucose concentrations within the normal physiologic range is considered important because hyperglycemia has been associated with increased risk of infection, increased mortality in the ICU, and adverse neurologic outcome. The chest roentgenogram is obtained to verify the proper position of the endotracheal tube and the position of intravascular catheters and to diagnose pneumothorax, atelectasis, pleural effusions, or pulmonary edema. Perioperative antibiotic prophylaxis is typically continued for 48 hours after surgery to decrease the risk of wound and endovascular infections.

THORACIC AORTIC ANEURYSM

An aortic aneurysm is a dilatation of the aorta containing all three layers of the vessel wall that has a diameter of at least 1.5 times that of the expected normal diameter of that given aortic segment. Thoracic aortic aneurysms are common, are detected in 10% of autopsies, have an incidence of 5.9 per 100,000 person-years, and are the most common reason for thoracic aortic surgery. The median age at the time of diagnosis is 65 years, and this lesion occurs two to four times more frequently in males. Common risk factors for thoracic aortic aneurysms include hypertension, hypercholesterolemia, prior tobacco use, collagen vascular disease, and family history of aortic disease. Thoracic aortic aneurysms are classified by their location, size, shape, and etiology. Among thoracic aortic aneurysms, descending thoracic aortic aneurysms are most common, followed by ascending aortic aneurysms, and less often by aortic arch aneurysms.

The anatomic location of the aneurysm and its extent determine its pathophysiologic consequences, operative approaches, and postoperative complications. Aneurysms involving the aortic root and ascending aorta are commonly associated with bicuspid aortic valve or aortic regurgitation (AR). Aneurysms extending into or involving the aortic arch require temporary interruption of cerebral blood flow to accomplish the operative repair. Endovascular stent repair is an option for aneurysms isolated to the descending thoracic aorta ending above the diaphragm. Repair of descending TAAAs requires the sacrifice of some or all of the segmental intercostal arteries branches and is associated with a risk of postoperative paraplegia from spinal cord ischemia or infarction. Aneurysmal disease of the thoracic aorta is often a diffuse process affecting multiple segments of the aorta and producing vessel tortuosity and often coexists in combination with isolated aneurysms of the abdominal aorta.

Most thoracic aortic aneurysms are asymptomatic and discovered incidentally through screening or as a consequence of medical workup for other cardiovascular disease (Box 17-1). The most common initial symptoms of thoracic aortic aneurysm are chest or back pain caused by aneurysmal expansion, rupture, or bony erosion. The mass effect of the aneurysm can cause hoarseness from stretching or compression of the recurrent laryngeal nerve, atelectasis from compression of the left lung, superior vena cava syndrome from compression of the superior vena cava or innominate vein, dysphagia from compression of the esophagus, or dyspnea from compression of the trachea, main stem bronchus, or pulmonary artery. Other symptoms include wheezing, cough, hemoptysis, or hematemesis. Aneurysm of the aortic root causing AR may present as dyspnea on exertion, heart failure, or pulmonary edema. Atherosclerotic aneurysms with mural thrombus may present as embolism, stroke, mesenteric ischemia, renal insufficiency, or limb ischemia.

BOX 17-1 Potential Complications of Thoracic Aortic Aneurysms

• Rupture

• Aortic regurgitation

• Trachea or left main stem bronchial compression

• Right pulmonary artery or right ventricular outflow tract obstruction

• Esophageal compression

Leakage or rupture of thoracic aortic aneurysms should be treated as a surgical emergency. Expansion and impending rupture are often heralded by the development of new or worsening pain, often of sudden onset. Rupture is accompanied by the dramatic onset of excruciating pain and hypotension. Rupture of an ascending aortic aneurysm into the pericardial sac causes cardiac tamponade. Rupture of a descending aortic aneurysm may cause hemothorax, aortobronchial fistula, or aortoesophageal fistula. If surrounding tissue does not contain a ruptured aortic aneurysm, the patient will exsanguinate and die.

General Surgical Considerations for Thoracic Aortic Aneurysms

The objective of surgical repair is to replace the aneurysmal segment of aorta with a tube graft to prevent morbidity and mortality as a consequence of aneurysm rupture. Indications for operative repair include the presence of symptoms refractory to medical management, evidence of rupture, an aneurysm diameter of 5.0 to 5.5 cm for an ascending aortic aneurysm, an aneurysm diameter of 6.0 to 7.0 cm for a descending thoracic aneurysm, or an increase in aneurysm diameter greater than or equal to 10 mm/yr. Earlier surgical intervention may be justified in patients with Marfan syndrome, a family history of aortic disease, or dissection. In several series, 1-, 3-, and 5-year survival was as high as 65%, 36%, and 20% for medically treated patients with thoracic aortic aneurysms, respectively. Aneurysm rupture may account for up to 32% to 47% of deaths.³

An important factor that dictates how the surgical repair is performed is the location and extent of the thoracic aortic aneurysm. Thoracic aortic aneurysms of the ascending aorta and aortic arch are approached from a median sternotomy incision. Standard CPB can be used for the repair of aneurysms limited to the aortic root and ascending aorta that do not extend into the aortic arch by cannulating the distal ascending aorta or proximal aortic arch and applying an aortic cross-clamp between the aortic cannula and the aneurysm. Aneurysms that involve the aortic arch require CPB with temporary interruption of cerebral perfusion. Neuroprotection strategies that involve a combination of deliberate hypothermia, selective ACP, and RCP are important to protect the brain from ischemic injury during reconstruction of the aortic arch. Aortic aneurysms that involve the descending thoracic aorta are approached from a lateral thoracotomy or thoracoabdominal incision. Reconstruction of the descending thoracic aorta can be accomplished without extracorporeal circulation by cross-clamping the thoracic aorta or with extracorporeal circulation using partial left-sided heart bypass to provide distal aortic perfusion. Partial left-sided heart bypass is accomplished through cannulation of the left atrium via a left pulmonary vein and cannulation of the distal aorta, internal iliac artery, or femoral artery. If the descending thoracic aortic aneurysm extends into the distal aortic arch, DHCA may be necessary to construct the proximal aortic anastomosis. Operations for descending thoracic aortic aneurysms require consideration of strategies to protect the mesenteric organs, spinal cord, and lower extremities from ischemia as a consequence of temporary interruption of organ blood flow or the sacrifice of collateral vessels to accomplish the repair.

Surgical Repair of Ascending Aortic and Arch Aneurysms

The surgical options for repair of ascending aortic aneurysms depend on the presence of aortic valve disease, aneurysm of the sinuses of Valsalva, and distal extension of the aneurysm into the aortic arch. Intraoperative TEE is useful for evaluating the aortic valve to determine if a valve-sparing surgery is feasible, to determine the aortic valve annular diameter in relation to the diameter of the sinotubular junction to assess aneurysmal dilation of the aortic root, and to detect and quantify the presence of AR after valve repair. The most common aortic valve diseases associated with ascending aortic aneurysm are bicuspid aortic valve or AR caused by dilation of the aortic root (Fig. 17-1). If the aortic valve and aortic root are normal, a simple tube graft can be used to replace the ascending aorta. If the aortic valve is diseased but the sinuses of Valsalva are normal, an aortic valve replacement combined with a tube graft for the ascending aorta without need for re-implantation of the coronary arteries can be performed. If disease involves the aortic valve, aortic root, and ascending aorta, the options include tube graft of the ascending aorta in combination with aortic valve repair, reconstruction of the aortic root with sparing or repair of the aortic valve, bioprosthetic aortic root replacement, composite valve/graft conduit aortic root replacement (Bentall procedure), or replacement of the aortic root with a pulmonary autograft (Ross procedure). Replacement of the aortic root requires re-implantation of the coronary arteries or aortocoronary bypass grafting (Cabrol technique). If there is evidence of significant coronary artery disease, a combined ascending aortic aneurysm repair and coronary artery bypass grafting (CABG) may be necessary.

Figure 17-1 A, TEE midesophageal long-axis image of the aortic valve demonstrating aneurysmal dilation of the aortic root and ascending aorta. B, Doppler color flow imaging demonstrating severe aortic regurgitation caused by outward tethering of the aortic valve cusps by the aortic aneurysm. LV = left ventricle; Ao = aorta.

Anesthetic Management for Ascending Aorta and Arch Aneurysms

The conduct of general anesthesia for repair of ascending aortic aneurysms requires attention to a number of specific concerns. A large ascending aortic aneurysm can cause a mediastinal mass effect. Computed tomographic or magnetic resonance imaging studies should be reviewed to assess for aneurysm compression of the right pulmonary artery, right ventricular outflow tract, trachea, or left main stem bronchus. A right radial arterial catheter is preferred for most cases. If arterial cannulation of the right axillary, subclavian, or innominate artery is planned for CPB or selective cerebral perfusion, bilateral radial arterial catheters are often necessary to measure cerebral and systemic perfusion pressures. Nasopharyngeal, tympanic, and bladder temperatures are important for estimating brain and core temperatures for monitoring the conduct of deliberate hypothermia and DHCA. EEG, SSEP, or oximetric jugular bulb venous oxygen saturation monitoring is sometimes useful for assessing cerebral metabolic activity for the conduct of DHCA. Control of the arterial pressure and prevention of hypertension are important to decrease left ventricular afterload in patients with AR and to decrease the risk of aneurysm rupture or expansion during induction of general anesthesia and surgical exposure. In patients with AR, antihypertensive drugs that decrease heart rate or myocardial contractility should be used cautiously to avoid heart failure. Intraoperative TEE is useful for evaluating the aortic valve and aortic root to determine the need for aortic root replacement or the feasibility of aortic valve repair. In patients with AR, a left ventricular vent is necessary to prevent ventricular distention during CPB. Patients with AR also require direct coronary cannulation for delivery of antegrade cardioplegic solution or a coronary sinus catheter to provide retrograde cardioplegia.

Neuroprotection Strategies for Temporary Interruption of Cerebral Blood Flow

Thoracic aortic surgery requiring temporary interruption of cerebral perfusion has been associated with the highest incidence of brain injury in comparison to other cardiac operations. Many reports assessing the incidence of neurologic injury were based on retrospective data collection or clinically diagnosed stroke. These reports suggest an incidence of stroke in the range of 7% to 9%. Studies that included a more detailed neurologic assessment and neuropsychological testing have found that neurologic deficits were more frequent in older patients and those subjected to DHCA for >25 minutes.⁴

Two major mechanisms are believed to explain the high incidence of stroke and neurocognitive dysfunction related to thoracic aortic operations. The first is cerebral ischemia or infarction caused by hypoperfusion or the need for temporary circulatory arrest during reconstruction of the aortic arch. The second is cerebral ischemia or infarction caused by cerebral embolization as a consequence of extracorporeal circulation or intrinsic vascular disease. Arterial emboli causing stroke can originate from multiple sources during thoracic aortic operations and include air introduced into the circulation from open cardiac chambers, vascular cannulation sites, or arterial anastomosis. Atherosclerotic or particulate debris may be released during clamping and unclamping of the aorta, the creation of anastomoses in the ascending aorta and aortic arch, or the excision of severely calcified and diseased cardiac valves. CPB may result in the generation of platelet aggregates, fat particles, and other microparticulate debris. The turbulent high-velocity blood flow out of the aortic cannula employed for CPB may also dislodge atherosclerotic debris within the aorta. Retrograde blood flow through a diseased descending thoracic aorta as a consequence of CPB conducted with femoral artery cannulation may cause retrograde cerebral embolization. For all these reasons, strategies to provide neurologic protection are important in the conduct of thoracic aortic operations (Box 17-2).

BOX 17-2 Brain Protection for Aortic Arch Reconstruction

• Deep systemic hypothermia

• Topical cerebral cooling

• Retrograde cerebral perfusion

• Selective antegrade cerebral perfusion

• Prevent cerebral hyperthermia during rewarming

Deep Hypothermic Circulatory Arrest

The brain is exquisitely susceptible to ischemic injury within minutes after the onset of circulatory arrest because it has a high metabolic rate, continuous requirement for metabolic substrate, and limited reserves of high-energy phosphates. In the 1970s, deep hypothermia and circulatory arrest were introduced to protect the brain from ischemic injury for operations on the aortic arch requiring temporary interruption of cerebral blood flow. The physiologic basis for deep hypothermia as a neuroprotection strategy is to decrease cerebral metabolic rate and oxygen demands to increase the period of time that the brain can tolerate circulatory arrest. Existing evidence indicates that autoregulation of cerebral blood flow is maintained during deliberate hypothermia with alpha-stat blood gas management. In adults, a 10°C decrease in body temperature decreases cerebral metabolic rate by an average factor of 2.6, a factor commonly referred to as the Q₁₀ ratio. Assuming an ischemic tolerance of 3 to 5 minutes under normothermic conditions, a Q₁₀ ratio of 2.6 predicts an ischemic tolerance in the range of 20 to 34 minutes at a brain temperature of 17°C or 53 to 88 minutes at a brain temperature of 7°C. More recent estimations of cerebral metabolism in adults undergoing DHCA suggest an ischemic tolerance of 30 minutes at 15°C and 40 minutes at 10°C.⁵ Direct measurement of cerebral metabolites and brainstem electrical activity in adults undergoing DHCA with RCP at 14°C indicated the onset of cerebral ischemia after only 18 to 20 minutes. It is also possible that hypothermia provides brain protection through mechanisms other than the reduction in cerebral metabolic rate. Despite an incomplete understanding of the mechanism and efficacy of hypothermia for cerebral protection, the large body of experimental evidence and clinical experience with the deliberate hypothermia suggest that it is the single most important intervention for preventing neurologic injury in response to circulatory arrest.

Despite the proven efficacy of hypothermia for operations that require circulatory arrest, no consensus exists on an optimal protocol for the conduct of deliberate hypothermia for circulatory arrest. The average nasopharyngeal temperature used for DHCA in several reported clinical series was 18°C, but the optimal temperature for DHCA has not been established. One problem with establishing the optimal temperature for DHCA is the inability to measure directly the brain temperature. In a study using EEG monitoring to establish physiologic criteria for cerebral metabolic suppression in response to hypothermia, the median nasopharyngeal temperature that electrocortical silence was achieved was 18°C, but a nasopharyngeal temperature of 12.5°C was necessary to ensure that 99.5% of patients achieved electrocortical silence.

The conduct of DHCA has several potential adverse sequelae. Lowering the target brain temperature extends the duration of CPB necessary for cooling and rewarming and all the problems inherent with prolongation of CPB such as injury to blood elements and the potential for cerebral embolization. Rewarming increases cerebral metabolic rate and has the potential to make the brain more vulnerable to ischemic injury, particularly during reperfusion after circulatory arrest. For these reasons, strategies to decrease the risk of brain injury during rewarming include delaying the start of rewarming by a period of hypothermic reperfusion, maintaining a temperature gradient of no more than 10°C in the heat exchanger, preventing the nasopharyngeal temperature from exceeding 37.5°C, or incomplete rewarming. Systemic hypothermia has commonly been associated with coagulopathy and increased risk of bleeding, but it has not been firmly established whether hypothermia is the underlying etiology of coagulopathy and bleeding. It is possible that systemic bleeding is a consequence of prolonged surgery, blood transfusion therapy, and intravascular volume expansion.

Retrograde Cerebral Perfusion

In 1990, RCP was reported as a means to deliver metabolic substrate to the brain during operations involving the aortic arch that required the interruption of ACP. RCP is performed by infusing cold oxygenated blood into the superior vena cava cannula at a temperature of 8°C to 14°C via the CPB machine. The internal jugular venous pressure is maintained at less than or equal to 25 mmHg to prevent cerebral edema. Internal jugular venous pressure is measured from the introducer port of the internal jugular venous cannula at a site proximal to the superior vena cava perfusion cannula and zeroed at the level of the ear. The patient is positioned in 10 degrees of Trendelenburg to decrease the risk of cerebral air embolism and prevent trapping of air within the cerebral circulation in the presence of an open aortic arch. RCP flow rates of 200 to 600 mL/min can usually be achieved. The potential benefits of RCP for neuroprotection include prolonging the safe period of DHCA by providing some metabolic substrate delivery to the brain, flushing embolic material from the cerebral arterial vasculature to decrease the risk of cerebral embolization on resuming ACP, and providing a means to maintain cerebral hypothermia during DHCA.^6,⁷

Pharmacologic Neuroprotection Strategies for Deep Hypothermic Circulatory Arrest

There are no proven pharmacologic regimens that have demonstrated effectiveness for decreasing the risk or severity of neurologic injury in the setting of thoracic aortic operations. Barbiturates or other central nervous system depressants decrease cerebral oxygen consumption and in theory offer the potential for cerebral protection in the setting of incomplete ischemia. Experimental studies and several clinical series support the administration of high-dose glucocorticoid to protect against cerebral and end-organ injury in the setting of DHCA, leading to the routine intravenous administration of methylprednisolone, 1 g, or dexamethasone, 100 mg, to patients undergoing thoracic aortic operations that require DHCA at many centers. Other unproved pharmacologic adjuncts that are routinely administered intravenously in an effort to provide organ protection in the setting of thoracic aortic operations requiring DHCA include magnesium sulfate, 1 to 2 g, lidocaine, 200 mg, or mannitol, 25 g. In general, the existing evidence suggests that pharmacologic neuroprotection is unreliable and should not be considered a substitute for hypothermia to protect against cerebral ischemia in the setting of hypoperfusion.

DESCENDING THORACIC AND THORACOABDOMINAL AORTIC ANEURYSMS

The objective of surgical repair for descending thoracic aortic aneurysms or TAAAs is to replace the diseased portion of the aorta with a prosthetic tube graft. The surgical approach to repair is through a lateral thoracotomy or thoracoabdominal incision. Despite technologic improvements, major challenges remain in the surgical management of patients with TAAA. The major etiology of this disease is atherosclerosis, and the typical patient requiring surgery often is elderly with coexisting peripheral vascular disease, cerebral vascular disease, renal vascular disease, coronary artery disease, and frequently chronic obstructive pulmonary disease from a history of tobacco use. Patients are particularly susceptible to renal, mesenteric, and lower extremity ischemia as a consequence of thromboembolic disease, the temporary interruption of blood flow to these organs, reperfusion injury, and difficulties encountered in the reconstruction of branch vessel anastomosis during the course of surgical repair. The need for a thoracoabdominal incision, division of the diaphragm, and surgical dissection in the proximity of the phrenic nerve, recurrent laryngeal nerve, and the esophagus represents major physiologic trespasses that increase the risk of postoperative wound dehiscence, respiratory failure, and dysphagia and is associated with a prolonged convalescence in many patients. Finally, the inability to identify or reattach all intercostal arteries to accomplish the repair decreases the vascular collateral supply to the spinal cord, making postoperative paraplegia a recognized complication of these operations. As a consequence of these medical, physiologic, and surgical challenges, repair of TAAA is considered a high-risk procedure and associated with high morbidity and mortality that vary depending on the hospital volume and surgical experience. In a nationwide sample of 1542 patients, the overall average mortality rate associated with TAAA repair was 22.3% with a cardiac complication rate of 14.8%, pulmonary complication rate of 19%, and acute renal failure rate of 14.2%.

Thoracic aortic aneurysms and TAAAs are classified according to the anatomic extent of the aneurysmal segment. The most commonly used classification scheme is that described by Crawford that categorizes aneurysm extent into four major groups (Fig. 17-2). Extent I TAAA involves the entire descending thoracic aorta from the origin of the left subclavian artery down to the level of the diaphragm ending above the renal arteries. Extent II TAAA involves the entire descending thoracic aorta with extension across the diaphragm into and through the abdominal aorta all the way to the aortic bifurcation. Extent III TAAA involves the distal half of the descending thoracic aorta, crosses the diaphragm, and involves most of the abdominal aorta. Extent IV TAAA is confined to the upper abdominal aorta.

Figure 17-2 Crawford classification of extent of thoracoabdominal aortic aneurysm.

(From Coselli JS: Descending thoracoabdominal aortic aneurysms. In Edmunds LH [ed]: Cardiac Surgery in the Adult. New York, McGraw-Hill, 1997, p 1232.)

Surgical repair of TAAA with an interposition tube graft can be accomplished by three major techniques that are used in varying degrees at different centers. The original technique for repair was accomplished by cross-clamping the thoracic aorta proximal to the aneurysm. The simple cross-clamp technique was subsequently refined by the application of arterial shunting (Gott shunt) or partial left-sided heart bypass using extracorporeal circulation to provide distal aortic perfusion while the proximal descending thoracic aorta was cross-clamped. The third technique is to perform the repair using DHCA alone or in combination with retrograde perfusion or selective antegrade perfusion of the brain or mesenteric organs. With all of the techniques, an attempt is usually made to reattach intercostal, lumbar, and sacral arteries to the graft to decrease the risk of spinal cord ischemia. Endovascular stent repair is now the fourth option, and clinical trials to assess its safety and efficacy are well under way.

Simple Aortic Cross-Clamp Technique

In 1965, Crawford developed the technique of aortic cross-clamping for TAAA repair and subsequently reported a mortality rate of 8.9% in more than 600 TAAA cases repaired with the simple cross-clamp technique. Mortality and paraplegia were related to the position and length of the resected aorta, the condition of the patient at the time of presentation, and the duration of time that the aorta was cross-clamped. A major disadvantage of the simple cross-clamp technique is the obligatory ischemic period to the body and organs distal to the aortic cross-clamp. For this reason, when the simple cross-clamp technique is used, the surgeon must clamp and sew as quickly as possible to limit ischemia time to the spinal cord and distal aortic territory. Theincidence of paraplegia and renal failure has been observed to correlate with the duration of the aortic cross-clamp time and was increased significantly for aortic cross-clamp times greater than 30 minutes. Other disadvantages associated with cross-clamping the descending thoracic aorta include proximal aortic hypertension, bleeding from arterial collaterals, and hemodynamic instability on reperfusion. Proximal aortic hypertension during the period that the aorta is cross-clamped may be poorly tolerated in patients with abnormal left ventricular function, regurgitant cardiac valve disease, or ischemic coronary artery disease. Blood loss as a result of bleeding from arterial collateral vessels can be minimized by the use of intraoperative red blood cell salvaging. Hemodynamic instability during release of the aortic cross-clamp and reperfusion often has to be managed with correction of metabolic acidosis, rapid intravascular volume expansion, vasopressor therapy, or the intermittent reapplication and gradual release of the aortic cross-clamp. Adjuncts to protect end-organ function from ischemia during aortic cross-clamping include mild deliberate hypothermia and selective cooling of the spinal cord. Despite the physiologic consequences, the aortic cross-clamp technique remains a relatively simple technique with proven clinical outcomes and is still favored by many surgeons (Table 17-3).

Table 17-3 Advantages and Disadvantages of Distal Perfusion Techniques for Thoracic or Thoracoabdominal Aortic Reconstruction

Potential Disadvantages

• Require greater level of systemic anticoagulation

• Increase risk of vascular injury at cannulation sites

• Increase risk of thromboembolic events

• Require perfusion team

• Need to monitor and control upper- and lower-body arterial pressure and flow

• Increase technical complexity of operation

Gott Shunt

Passive shunting of blood from the proximal to distal aorta has been used to provide distal aortic perfusion during aortic cross-clamping for TAAA repair. A Gott shunt is a tapered heparin-coated tube designed so that both ends can serve as arterial cannulas. The ascending aorta or aortic arch can serve as the proximal cannulation site for the Gott shunt. The distal descending thoracic aorta, iliac artery, or femoral artery can serve as the distal cannulation site for the Gott shunt. Blood flow from the proximal to distal aorta through the Gott shunt is variable and governed by the proximal aortic pressure, diameter and length of the shunt, and distal aortic pressure. Monitoring the distal aortic pressure through a femoral arterial catheter can be used to assess distal aortic perfusion and shunt flow. Advantages of the Gott shunt are that it is simple, inexpensive, requires only partial anticoagulation, and does not require perfusion personnel. Disadvantages of the Gott shunt include technical difficulty with cannulation in some patients, vessel injury, dislodgment, bleeding from the cannulation site, embolic stroke, and unproven efficacy for the prevention of paraplegia and end-organ dysfunction. An alternative technique to provide passive distal aortic perfusion is to perform an axillofemoral bypass before aortic cross-clamping.

Partial Left-Sided Heart Bypass

Partial left-sided heart bypass with extracorporeal circulation is a method of controlling both proximal aortic and distal aortic perfusion during aortic cross-clamping for TAAA repair. The technique of partial left-sided heart bypass involves cannulation of the left atrium from a left thoracotomy incision usually via a left pulmonary vein. Oxygenated blood from the left atrium is directed through the extracorporeal circuit with a centrifugal pump and into an arterial cannula placed in either the distal aorta, iliac artery, or femoral artery.⁸ The extracorporeal circuit used to provide partial left-sided heart bypass can be modified in a number of ways to include or not include a heat exchanger, membrane oxygenator, or venous reservoir. Heparin requirements for partial left-sided heart bypass range from minimal to no heparin when heparin-coated circuits without oxygenators are used to full systemic anticoagulation with activated coagulation time greater than 400 seconds when circuits with membrane oxygenators and heat exchangers are used. During partial left-sided heart bypass, the mean arterial pressure in the proximal aorta monitored by a radial arterial catheter is generally maintained in the range of 90 mmHg. Bypass flow rates in the range of 1.5 to 2.5 L/min are usually necessary to maintain a distal aortic mean arterial pressure in the range of 60 to 70 mm Hg measured through a femoral arterial catheter.⁹ Sequential advancement of the distal aortic cross-clamp during partial left-sided heart bypass after successive reattachment of intercostal arteries, mesenteric artery, and the renal arteries to the graft permits segmental reconstruction of the thoracoabdominal aorta to decrease end-organ ischemia. Advantages of partial left-sided heart bypass include the ability to control proximal aortic and distal aortic perfusion pressures, control systemic temperature with a heat exchanger, provide reliable perfusion to the lower body and mesenteric organs, permit selective cannulation and antegrade perfusion of mesenteric branch vessels, and preserve lower extremity somatosensory and motor nerve function for intraoperative neurophysiologic monitoring. Two contemporary clinical series have suggested that use of partial left-sided heart bypass was protective against postoperative paraplegia.¹⁰ Disadvantages to partial left-sided heart bypass include increased expense, increased complexity, and requirement for systemic anticoagulation (see Table 17-3).

Cardiopulmonary Bypass and Deep Hypothermic Circulatory Arrest

Full CPB and DHCA has been described for TAAA repair with acceptable morbidity.¹¹ DHCA is necessary for construction of the proximal graft anastomosis if the aneurysm extends into the distal aortic arch or if the proximal descending aorta cannot be cross-clamped because the aorta is heavily calcified or cross-clamping compromises flow in the left common carotid artery. DHCA has also been advocated as an alternative method to protect the spinal cord and mesenteric organs from ischemia before the reattachment of branch vessels. If full CPB and DHCA are planned for TAAA repair through a left thoracotomy incision, preoperative echocardiography or intraoperative TEE is necessary to evaluate for the presence of AR so that a left ventricular vent can be inserted during surgery to prevent overdistention of the left ventricle with the onset of asystole during deliberate hypothermia. DHCA has the advantage of providing a bloodless surgical field for open anastomosis. Potential disadvantages of CPB and DHCA is the limited safe period for circulatory arrest, risk of stroke from cerebral embolization caused by retrograde perfusion of the aortic arch through a diseased descending thoracic aorta, increased duration of CPB for deliberate hypothermia and rewarming, and possibly increased risk of bleeding from hypothermia.

Endovascular Stent Graft Repair of Thoracic Aortic Aneurysms

Endovascular stent grafts are fabric or synthetic tube grafts reinforced by a wire frame that can be collapsed within a catheter for delivery and deployment within the aortic lumen. The endovascular stent graft is designed to be deployed within the aorta to span the length of the aneurysm and exclude blood flow into the aneurysm cavity. Endovascular stent graft repair for thoracic aortic aneurysms has been reported for the repair of isolated descending thoracic aortic aneurysms, repair of distal aortic arch aneurysms with partial arch reconstruction, and a few cases of transverse aortic arch aneurysms with dissection.¹² Endovascular stent repair requires the existence of a 1-cm-long nontapered region of aorta on either end of the aneurysm, often called the aneurysm neck, to provide a landing zone for each end of the graft. Furthermore, aneurysms that span essential aortic branch vessels require extra-anatomic bypass of those vessels before endovascular stent grafting.

Long-term results and efficacy of endovascular stent repair of thoracic aortic aneurysms remain to be determined. Problems that have been encountered with endovascular stent graft repair include vessel injury caused by the delivery catheter, intravascular migration of the graft, strut fracture of the stent frame, postoperative paraplegia, and endovascular leak at the graft ends, between graft segments, or from segmental arteries within the aneurysm cavity.

Anesthetic Management for Thoracoabdominal Aortic Aneurysm Repair

The anesthetic management of patients undergoing TAAA repair requires several special considerations. Selective one-lung ventilation is required for left thoracotomy or thoracoabdominal incision. Paraplegia is a major complication of the procedure, and an important aspect of the anesthetic management is directed toward strategies to decrease the risk of postoperative paraplegia from spinal cord ischemia in high-risk patients. A right radial arterial catheter is preferred to monitor proximal aortic pressure if the aortic cross-clamp has to be applied across the left subclavian artery or if the left brachial artery has to be accessed for endovascular stent graft deployment. A femoral artery or distal aortic cannula is necessary to measure distal aortic perfusion pressure for partial left-sided heart bypass or when a Gott shunt is used. Hemodynamic monitoring of the central venous pressure, pulmonary artery pressure, and cardiac output is useful for managing the circulation during proximal aortic cross-clamping, distal aortic reperfusion, partial left-sided heart bypass, or partial CPB. Intraoperative neurophysiologic monitoring with SSEPs or MEPs for the detection of spinal cord ischemia requires specific attention to the types and doses of anesthetic agents used for the operation. Perioperative renal insufficiency from mesenteric ischemia may complicate intravascular fluid and electrolyte management and require adjustment in the dose of drugs cleared by renal excretion. Left thoracotomy, thoracoabdominal incision, division of the diaphragm, and dissection near the recurrent laryngeal and phrenic nerve increase the risk of postoperative respiratory failure and aspiration pneumonia. Postoperative pain is also an important concern, and effective postoperative pain management by intravenous analgesics or epidural analgesia may improve pulmonary function.

Lung Isolation Techniques

Selective right lung ventilation is required for left thoracotomy or left thoracoabdominal approach to TAAA repair. Selective ventilation of the right lung and collapsing the left lung during TAAA repair improves surgical exposure and decreases the risk of pulmonary contusion or torsion of the left lung. One-lung ventilation also serves to protect the right lung in the event of hemoptysis or bleeding from the left lung. Although it is possible to accomplish TAAA repair with a single-lumen endotracheal tube and lung retraction, anesthetic techniques to provide one-lung ventilation are always preferable.

Two major techniques are available to provide one-lung ventilation. The first is selective endobronchial intubation with a double-lumen endobronchial tube. The second is the use of a bronchial blocker. The routine use of fiberoptic bronchoscopic guidance has increased the reliability of achieving satisfactory lung isolation with either of the techniques. Although a right or left endobronchial double-lumen endotracheal tube can be used for lung isolation, a left-sided endobronchial tube is used most commonly. The increased length of the left main stem bronchus makes it easier to properly position the endobronchial lumen of a left-sided double-lumen tube and makes it less prone to dislodgment or malposition during surgery. Commercially available integrated airway devices (Arndt blocker, Cohen blocker, or Univent tube) to accomplish endobronchial blockade has also improved the ease and reliability of this technique compared with improvisation using a Fogarty balloon-tipped catheter. Wire-guided endobronchial blocking catheters permit the balloon-tipped catheter to be guided and positioned precisely in the left main stem bronchus with a fiberoptic bronchoscope.

Paraplegia after Thoracoabdominal Aortic Aneurysm Repair

The most devastating complication of TAAA repair is postoperative paraplegia caused by spinal cord ischemia and infarction. Although the exact pathophysiology and clinical events that lead to paraplegia after TAAA repair are incompletely understood, temporary interruption of distal aortic perfusion and sacrifice of intercostal and segmental arteries to accomplish TAAA repair are central events that predispose the spinal cord to ischemia and subsequent infarction. The incidence of paraplegia or paraparesis after TAAA repair based on clinical series reported in the literature varies widely and ranges from 2.9% to 32%. Factors believed to contribute or influence the risk of postoperative paraplegia include the extent of the TAAA, acute presentation, aneurysm rupture, the duration of ischemia as a consequence of aortic cross-clamping, the loss of critical intercostal arteries, the presence of dissection, the surgical technique used to accomplish the repair, and the use of techniques to protect the spinal cord.¹³ The extent of the neurologic deficit in paraplegia or paraparesis varies from patient to patient but typically extends from the lumbosacral cord to the mid- to high thoracic level. Postoperative paraplegia is particularly poorly tolerated in elderly patients, is associated with respiratory insufficiency, and has a mortality rate that ranges from 63% to 100% depending on the length of follow-up. Although controversial, it is likely that perioperative management strategies directed at the detection and treatment of spinal cord ischemia have the potential to decrease the risk of paraplegia after TAAA repair (Table 17-4.)

Table 17-4 Strategies to Decrease the Risk of Paraplegia from Spinal Cord Ischemia after Thoracic or Thoracoabdominal Aortic Procedures

Minimize Aortic Cross-Clamp Time

Distal aortic perfusion

Passive shunt (Gott)

Partial left-sided heart bypass

Partial cardiopulmonary bypass

Deliberate Hypothermia

Mild-to-moderate systemic hypothermia (32°C to 35°C)

Deep hypothermic circulatory arrest (14°C to 18°C)

Selective spinal cord hypothermia (epidural cooling, 25°C)

Increase Spinal Cord Perfusion Pressure

Re-implantation of critical intercostal and segmental arterial branches

Lumbar cerebrospinal fluid drainage (CSF pressure ≤ 10 mmHg)

Arterial pressure augmentation (MAP ≥ 85 mmHg)

Intraoperative Monitoring of Lower Extremity Neurophysiologic Function

Somatosensory evoked potentials (SSEPs)

Motor evoked potentials (MEPs)

Postoperative Neurologic Assessment for Early Detection of Delayed-Onset Paraplegia

Serial neurologic examinations

Pharmacologic Neuroprotection

Glucocorticoid

Barbiturate or central nervous system depressants

Magnesium sulfate

Mannitol

Naloxone

Lidocaine

Intrathecal papaverine

The anatomic distribution of arteries that supply the spinal cord provides a partial explanation of the risk and clinical features of postoperative paraplegia after TAAA repair. The anterior spinal artery supplies the anterior two thirds of the spinal cord, and a pair of posterior spinal arteries supplies the posterior third of the spinal cord. Branches from each vertebral artery join to form the anterior spinal artery that descends along the midline of the anterior surface of the spinal cord. As it descends, the anterior spinal artery is sometimes discontinuous and fed in a variable extent by radicular arteries derived from ascending cervical, deep cervical, intercostal, lumbar, and sacral segmental arteries. The paired posterior spinal arteries also branch off the vertebral arteries and receive flow to a varying extent from posterior radicular arteries. The terminal region of the spinal cord and the caudal extent of the anterior and posterior spinal arteries are supplied by radicular arteries that arise from the internal iliac, lateral sacral, iliolumbar, and middle sacral arteries. The thoracic and lumbosacral regions of the spinal cord often receive blood supplied from more than one arterial source and are particularly vulnerable to ischemia if suddenly deprived of blood from one of the sources. In these watershed regions, blood supply from one or several large radicular arteries may be crucial. In some patients, a particularly large radicular artery arising from an intercostal artery between T9 and T12 in 75% of patients, T8 to L3 in 15%, and L1 to L2 in 10%, often called the arteria magna or artery of Adamkiewicz, can be identified. Based on the anatomic distribution of vessels supplying the spinal cord, temporary or permanent disruption of flow to the segmental arteries arising from the descending thoracic aorta can make the spinal cord vulnerable to ischemia and subsequent infarction.

Postoperative paraplegia can be subdivided into those with immediate-onset paraplegia and those with delayed-onset paraplegia. Delayed-onset paraplegia accounts for 30% to 70% of patients with postoperative paraplegia or paraparesis. The extent of the neurologic deficit often varies among patients. In patients with postoperative neurologic deficits, the incidence of paraplegia and paraparesis is equally divided. Infarction in the territory of the anterior spinal artery classically causes motor paralysis with preservation of proprioception or some sensory function, but clinical experience has demonstrated that the pattern of paraplegia and paraparesis after TAAA is variable and often asymmetric and can affect either or both motor and sensory function.

In immediate-onset paraplegia, the patient is paraplegic on emergence from general anesthesia after TAAA repair. Immediate-onset paraplegia is likely a consequence of spinal cord ischemia leading to infarction that occurred at some time during surgery while the patient was under general anesthesia. In contrast to delayed-onset paraplegia, recovery or response to treatment in immediate-onset paraplegia has not been consistently demonstrated. The lack of improvement in response to measures to improve spinal cord perfusion in immediate-onset paraplegia indicate that irreversible injury had already occurred by the time paraplegia was diagnosed. For this reason, strategies to prevent immediate-onset paraplegia are directed toward protection of the spinal cord from ischemia and infarction during surgery (Box 17-3). Intraoperative efforts to protect the spinal cord from ischemia include augmentation of the arterial pressure, lumbar CSF drainage, provision of distal aortic perfusion with partial left-sided heart bypass, minimization of the ischemic time, deliberate hypothermia, segmental reconstruction of the aorta, re-implantation of intercostal arteries, or pharmacologic neuroprotection. The objective of using intraoperative neurophysiologic monitoring during general anesthesia is to detect spinal cord ischemia to permit immediate interventions to improve spinal cord perfusion during general anesthesia. Distal aortic perfusion maintains spinal cord function during aortic cross-clamping and improves the ability to monitor spinal cord integrity during surgery with SSEPs or MEPs.

BOX 17-3 Techniques to Decrease the Risk of Intraoperative Spinal Cord Ischemia

• Mild systemic hypothermia

• Lumbar cerebrospinal fluid drainage

• Selective spinal cord cooling

• Distal aortic perfusion

• Intraoperative motor or somatosensory evoked potential monitoring

• Arterial pressure augmentation

BOX 17-4 Prevention and Treatment of Delayed-Onset Spinal Cord Ischemia

• Maintain mean arterial pressure ≥85 mmHg

• Serial neurologic assessment for lower extremity weakness or sensory loss

• Immediate treatment to augment spinal cord perfusion pressure

• Arterial pressure augmentation with vasopressor therapy

• Lumbar cerebrospinal fluid drainage

• Prevent hypotension

Postoperative Analgesia after Thoracoabdominal Aortic Aneurysm Repair

It is well recognized that thoracotomy and thoracoabdominal incision is very painful and may cause respiratory splinting and retention of airway secretions that may contribute to the development of postoperative respiratory failure. Epidural analgesia is a proven method of providing postoperative pain relief for thoracotomy, laparotomy, and other surgical incisions that span the regions innervated by the spinal nerves. Although the clinical efficacy of epidural analgesia for postoperative pain relief has not been specifically tested in patients undergoing TAAA repair, an effort is usually made to supplement systemic opioid analgesia with epidural analgesia to achieve patient comfort during convalescence. Furthermore, providing effective postoperative analgesia may permit patients to awake earlier after surgery for assessment and monitoring of neurologic function.

The usual management of epidural anesthesia and analgesia may need to be modified when applied to the patient undergoing TAAA repair because the complications of epidural analgesia are difficult to distinguish from postoperative paraplegia caused by spinal cord ischemia.¹⁷ The epidural analgesia regimen should be formulated to minimize interference with the ability to monitor lower extremity neurologic function and not cause sympathetic blockade that may contribute to postoperative hypotension. For example, bupivacaine 0.05% combined with fentanyl, 2 μg/mL, can be administered via a patient-controlled epidural analgesia infusion pump at a basal rate of 4 to 8 mL/hr initiated after surgery and after the patient exhibits normal neurologic function. Bolus administration of concentrated local anesthetic through the epidural catheter should be discouraged to avoid sympathetic blockade and associated hypotension. The epidural catheter can be inserted before, at the time of surgery, or in the postoperative period. Hemorrhagic complications attributed to epidural catheter insertion or removal have been rare, but care should be exercised to verify that the patient is not being treated with antiplatelet or anticoagulant drugs and that coagulation parameters are satisfactory before insertion and during removal of the epidural catheter.

AORTIC DISSECTION

Aortic dissection is caused by a tear in the intima of the aorta, exposing the underlying diseased medial layer to the pulsatile pressure of the blood within the aortic lumen. Blood exiting the true lumen of the aorta into the medial layer of the vessel through the intimal tear causes the intima to separate or dissect circumferentially and longitudinally within the aorta, creating a true and false lumen contained by the adventitia.¹⁸ The aortic dissection may remain localized to an isolated segment of the aorta at the primary entry site at the original intimal tear. Often, the aortic dissection extends distally along the length of the aorta starting at the primary entry site, but it can also propagate proximally or in a retrograde direction. As the dissection propagates along the length of the vessel, the dissection can extend into the aortic branch vessels, cause occlusion of branch vessels resulting in malperfusion syndromes, or the intima may shear at the site of branch vessels creating multiple fenestrations. Propagation of the dissection into the aortic root can cause AR. The development of a false lumen and weakening of the aortic wall caused by the dissection is often accompanied by dilation and expansion in the diameter of the aorta.

Thoracic aortic dissections can be classified according to the location and extent of the aortic dissection. There are two generally accepted classification schemes for thoracic aortic dissections (Table 17-5).

Table 17-5 Classification of Acute Aortic Dissection

DeBakey Classification

Type I: Involvement of entire aorta (ascending, arch, and descending)

Type II: Confined to the ascending aorta

Type III: Intimal tear originating in the descending aorta with either distal or retrograde extension

Type IIIA: Intimal tear originating in the descending aorta with extension distally to the diaphragm or proximally into the aortic arch

Type IIIB: Intimal tear originating in the descending aorta with extension below the diaphragm or proximally into the aortic arch

Stanford Classification

Type A: Involvement of the ascending aorta or aortic arch regardless of the site of origin or distal extent

Type B: Confined to the descending aorta distal to the origin of the left subclavian artery

Type A Aortic Dissection

Aortic dissections that involve the ascending aorta (Stanford type A) are considered surgical emergencies. From 60% to 70% of patients presenting with aortic dissection will have a Stanford type A dissection. According to an international registry for acute aortic dissection, mortality rates for patients with Stanford type A aortic dissection managed without surgery were estimated to be 1% to 2% per hour after the initial symptom onset and 1% per hour thereafter for the first 48 hours, 60% by day 6, 74% by 2 weeks, and 91% by 6 months.¹⁹ When managed with surgery, the mortality rate for type A aortic dissection was 26%. The causes of death and morbidity attributed to type A aortic dissection included rupture of the ascending aorta causing cardiac tamponade, myocardial ischemia or infarction when the dissection involves the coronary ostia, heart failure caused by acute AR, stroke caused by malperfusion of the aortic arch branch vessels, mesenteric malperfusion causing renal failure or ischemic bowel, or limb ischemia.²⁰ Aortic dissection can also rupture into the right atrium, the right ventricle, or the left atrium causing intracardiac shunting with congestive heart failure. An aortic dissection can be considered chronic after 2 weeks, because mortality tends to level off at that time. Late complications of type A aortic dissection include worsening AR, aneurysm formation, or aortic rupture.