Chapter 52. Aneurysms of the Aortic Arch

The critical consideration in approaching aortic arch (AA) surgery, how best to protect the brain while providing surgical access to the cerebral vessels, remains a subject of controversy and research, but involves two key aspects: minimizing cerebral ischemia and preventing cerebral embolization of air and atheromatous debris. Thus, this chapter focuses on the laboratory and clinical basis for cerebral protection methods; including methods for preventing cerebral ischemia, such as hypothermic circulatory arrest (HCA), selective antegrade perfusion (SCP), and retrograde cerebral perfusion (RCP); and methods to minimize embolic damage, such as using axillary artery cannulation plus a branched graft technique.

Urgent indications for AA surgery include rupture of an aneurysm, pseudoaneurysm, or aortic dissection. Elective arch surgery is recommended for aneurysms greater than 6 cm, saccular aneurysms with rapid enlargement (>1 cm/y) and for symptoms (pain or hoarseness). Smaller aneurysms (5 cm) should be considered for repair in patients with extensive aortic aneurysmal disease (ascending and descending), Marfan's syndrome, or a family history of rupture or dissection.

The medical history is important in identifying symptoms caused by an aneurysm and, along with routine laboratory studies, may help elaborate comorbidities in these often elderly patients. A family history of a ruptured aneurysm is not uncommon and aids in the decision to recommend surgery.1 Identifying comorbidities may influence the operative approach, allow anticipation, and prevention of complications, or may contraindicate surgery altogether.

Evaluation of an AA aneurysm requires a contrast-enhanced computed tomographic (CT) angiogram of the entire aorta. Multidetector CT scans permit rapid imaging of the entire aorta and three-dimensional reconstructions. Magnetic resonance imaging (MRI) yields equally detailed images but entails longer scanning time, higher cost, and the contrast agent, gadolinium, may be nephrotoxic. Angiograms are not routinely required; however, coronary angiography is usually indicated and visualization of the brachiocephalic vessels may be obtained at that time with little added risk.

Cardiac Status and Management of Coronary Artery Disease

All patients require a preoperative echocardiogram to assess left ventricular function (LVF) and exclude significant valvular heart disease. Coronary arteriography is carried out to delineate the anatomy of the proximal coronary arteries in patients with AA aneurysms in whom a Bentall or valve sparing procedure may be required; in patients older than 40; and in younger patients with risk factors, such as smoking, angina, a strong family history, an abnormal ECG or stress test.

Significant coronary artery disease may warrant angioplasty or coronary artery bypass surgery (CABG). Drug-eluting stents are not used for angioplasty, to avoid Plavix therapy, and the procedure is performed several weeks preoperatively, as stent thrombosis may complicate intraoperative protamine administration; antiplatelet therapy is discontinued. If technically feasible, CABG can be done at the time of aneurysm repair. However if a left thoracotomy is anticipated, making access to the coronary arteries difficult, CABG can be undertaken several weeks before aneurysmectomy.

Pulmonary dysfunction increases operative risk and prolongs recovery, but chronic lung disease is not necessarily a contraindication to surgery unless oxygen dependence or significant carbon dioxide retention is present. If limited exercise tolerance or abnormal pulmonary function tests suggest severe respiratory dysfunction, pulmonary consultation is warranted. Active pulmonary infection should be treated before surgery and active smokers are urged to stop smoking for at least a month before operation; smokers may require pulmonary rehabilitation.

Cerebral Vessels and Prevention of Stroke

Carotid and vertebral duplex ultrasonography is requested if there is a history of transient ischemic attacks or strokes or if carotid bruits are present. In patients with an aberrant left vertebral artery exiting the arch directly, documentation of the size and patency of the right vertebral artery is essential to guide strategy for complete arch replacement.

Although a history of a focal cerebral insult is not a contraindication to surgery, it warrants obtaining a preoperative CT scan to rule out silent, fresh cerebral infarcts, which generally necessitate postponing surgery. A preoperative head CT scan is also invaluable for identifying old and new lesions and may be helpful in determining prognosis if focal neurologic symptoms occur postoperatively.

Ascending and arch aneurysms often have friable atheromatous lesions, so all possible steps to minimize embolization must be taken. Preoperative identification of patients at high risk for embolization is possible using transesophageal echocardiography (TEE) and high-resolution CT angiography; epiaortic ultrasound may be especially useful (12-MHz probe) intraoperatively.

Cannulation Sites

Right axillary artery cannulation offers many advantages in the management of arch aneurysms.2 The axillary artery is usually soft and is rarely involved by generalized atherosclerosis or aortic dissection. As compared with ascending aortic cannulation, axillary cannulation avoids the dislodgement of debris associated with cannula insertion and debris dislodgement that results from turbulent arch flow. As compared with femoral cannulation, axillary perfusion avoids possible embolization resulting from retrograde flow through a diseased abdominal and descending aorta. Moreover, cannulating the femoral arteries, which are often calcified and atherosclerotic, is associated with the risk of local and retrograde dissection. In aortic dissection surgery, the risk of malperfusion is lower with axillary perfusion and it has been associated with improved outcomes.3,4 Axillary artery cannulation also facilitates selective antegrade cerebral perfusion, as discussed in the following.

Although many surgeons prefer a side branch technique for axillary perfusion, attaching an 8- or 10-mm graft to the artery,5 we prefer direct right axillary artery cannulation via a transverse arteriotomy using a right angle, wire-reinforced arterial cannula (Edwards Lifesciences, Irvine, CA).2 Depending on the adequacy of collateral circulation, direct cannulation may render the arm ischemic, so the period of cannulation should be limited and the cannula should be removed before protamine administration. In patients with very small axillary arteries, transecting the artery, sewing a 6-mm graft end to end proximally and then cannulating the graft with a straight femoral arterial cannula works well; on discontinuing cardiopulmonary bypass, the 6-mm graft may be used to reestablish continuity of the divided axillary artery. Right axillary cannulation is also possible in conjunction with a left thoracotomy (Fig. 52-1). A 10-mm ringed PTFE graft is sewn to the right axillary artery with the patient supine; with the incision loosely closed and the graft secured to the anterior chest with an Ioban drape (3M, St. Paul, MN), the patient is repositioned for a left thoracotomy, leaving the PTFE graft available for antegrade perfusion.

For procedures requiring a thoracotomy, particularly if substantial dissection and mobilization of the descending thoracic aorta is necessary before institution of cardiopulmonary bypass (CPB), use of a double-lumen tube, permitting selective ventilation, is helpful.

Anesthesia for aortic arch surgery, like anesthesia for most cardiac surgery, relies primarily on the use of high doses of narcotics. Routine hemodynamic monitoring includes left radial and femoral arterial catheters, a Swan-Ganz catheter, and a jugular venous bulb catheter, if possible. TEE is used to monitor LVF and distention, to confirm adequate flow in the arch and arch vessels, and to guard against malperfusion. Although we do not rely on electroencephalographic (EEG) surveillance, it is still used by some surgeons to determine maximum cerebral metabolic suppression in conjunction with HCA, and assess adequacy of cerebral protection.

Cerebral oximetry, used to monitor cerebral perfusion and oxygenation, is best followed by observing the baseline and trend rather than the absolute values. Both cerebral hemispheres are monitored and any asymmetric change should prompt a thorough assessment to determine the adequacy of cerebral blood flow. For example, if unilateral SCP via the right axillary is used, poor left hemispheric cerebral oximetry may indicate insufficient collaterals and the need for direct cannulation and perfusion of the left common carotid artery.6 Similarly, acute changes occurring with SCP administered via direct cannulation of the head vessels may indicate catheter migration (into the right subclavian artery), catheter obstruction, or dislodgement7 and should prompt immediate steps to identify and correct the problem. It should be noted that transcranial Doppler is more sensitive in detecting embolic events and confirming cerebral blood flow than cerebral oximetry,8 but is more operator-dependent and may not be available in emergent situations.9

Methylprednisolone (1 g) is administered on initiating CPB when HCA is anticipated. If HCA exceeds 30 minutes, steroids are given for 48 hours postoperatively (125 mg every 6 hours for 24 hours, then 125 mg every 12 hours for 24 hours). Barbiturates are not used because they significantly depress myocardial function at the doses recommended for cerebral protection, and may not be effective in the presence of hypothermia.10

Steroid administration and hypothermia-induced catecholamine release often produce hyperglycemia, which may adversely affect intracellular pH and neurologic outcome.11 Hyperglycemia should be treated aggressively, because glucose drives anaerobic glycolysis, leading to rapid accumulation of lactate and intracellular acidosis during HCA. We use an intravenous insulin drip to maintain normoglycemia intraoperatively and postoperatively.

Perfusion

The routine perfusion protocol for cardiac operations is used for repair of arch aneurysms. If axillary artery perfusion is used, CPB is initiated slowly, monitoring with TEE, while observing for adequacy of flow and signs of dissection or malperfusion. With median sternotomy right axillary artery perfusion can be used throughout the procedure, allowing retrograde flushing of the brachiocephalic vessels. However, for distal arch reconstruction via a left thoracotomy, placing a Y connector in the arterial line enables arterial perfusion to be transferred from the femoral artery to the proximal graft following deep HCA.

After HCA, an inline LG-6 leukocyte-depleting filter (Pall Corp., East Hills, NY) is used for both leukocyte depletion and ultrafiltration, to increase oxygen-carrying capacity.

During hypothermic perfusion, the advantages of regulating pH using the alpha-stat versus pH stat techniques are debated. We use values uncorrected for temperature, the alpha-stat approach, with a perfusate temperature between 15 and 20°C, a hematocrit of 25 to 30%, and flows of 8 to 10 cc/kg/min, and with a mean arterial pressure (MAP) of 40 to 60 mm Hg.

Nonpulsatile flow gradually increases cerebral vascular resistance, so higher pressures may be required for effective perfusion toward the end of a long bypass period, and immediately thereafter to avoid underperfusion. However, it should be noted that overperfusion has been shown to be as detrimental as underperfusion in a canine model.12 Evidence for SCP in adults indicates that alpha-stat regulation helps in preserving cerebral autoregulation, maintaining metabolic suppression, and reducing the risk of cerebral embolization.13 However, in patients with previous strokes, experimental studies suggest that the injured brain is susceptible to ischemia during SCP and the use of pH-stat management—which increases flow—may be marginally beneficial in this subset of patients.14

We rely on a long duration of cooling, a low esophageal temperature, a high jugular venous oxygen saturation, and topical hypothermia (ice packs on the head) to ensure adequate cerebral protection during HCA.

Incision

In most AA cases, an extended median sternotomy is used, giving access to the ascending aorta, arch, and proximal descending thoracic aorta as far as 5 cm beyond the left subclavian artery. The conventional median sternotomy is extended along the border of the left sternocleidomastoid muscle. The strap muscles of the left side of the neck may be incised, and the innominate vein is usually mobilized and preserved, but can be divided if necessary.

If the anticipated surgery involves intracardiac pathology and/or resection of extensive portions of the aorta, some surgeons advocate a thoracosternotomy or bilateral anterior thoracotomy incision.15 The bilateral anterior thoracotomy permits excellent exposure of the ascending aorta, arch, and most of the descending aorta, but may have a deleterious effect on pulmonary function; it involves sacrifice of both internal mammary arteries and puts both phrenic nerves at risk. We prefer to carry out aneurysm repair in two stages using an elephant trunk approach16–18 and reserve the thoracosternotomy incision for reoperations and patients requiring emergent correction of simultaneous cardiac and aortic arch/descending pathology. In patients with a lesion primarily in the descending aorta that extends no farther proximally than the distal arch, a left lateral thoracotomy in the fifth intercostal space is the incision of choice.

Cooling and Rewarming

We lower the perfusate temperature toward 10°C, and monitor both bladder and esophageal (or tympanic) temperatures. After HCA, the perfusate temperature to which the brain is exposed is critical.19 We use a period of hypothermic reperfusion, which our laboratory data have shown to significantly improve outcome, with a reproducible trend toward improved neurobehavioral and histologic outcomes.20 Conversely, in an animal model, hyperthermic reperfusion was associated with deterioration of neurologic and behavioral outcome, correlating with histologic evidence of significant brain injury.21

During rewarming, we never raise blood temperature above 37°C, and we avoid creating a gradient exceeding 10°C between the blood and esophageal temperatures. Warming is discontinued when the esophageal (or tympanic) temperature reaches 35°C and the bladder temperature reaches 32°C. We prefer the patient to rewarm gradually in the intensive care unit after closure.

Graft and Suture Materials and Anastomotic Technique

Generally, an aneurysm repair consists of complete excision and replacement with an impregnated Dacron graft. We construct full-thickness anastomoses to the remaining, normal aorta, creating a “sandwich” of the aortic wall, with Teflon felt outside and graft material invaginated within the lumen.22 Long-term follow-up of 2281 “sandwich” anastomoses, comprising 6484 patient-years, documents that pseudoaneurysm formation is extremely rare.22 Most anastomoses are constructed with 3-0 polypropylene. However, graft-to-graft anastomoses never truly heal, so 2-0 is used, because the lifetime integrity of these anastomoses depends on the sutures.

Myocardial Protection

Myocardial protection is achieved by administering antegrade and retrograde, cold blood cardioplegia, generally supplemented by the combined effects of total body hypothermia and topical hypothermia. When access for antegrade perfusion is difficult and HCA is to be used, asystole may be induced by infusing 60 mEq of potassium into the pump circuit, over 1 to 2 minutes, just before circulatory arrest.23

Prevention of Paraplegia

Although paraplegia is not a common complication of most AA operations, preventative precautions must be taken with procedures involving the descending thoracic and thoracoabdominal aorta. Total body hypothermia affords some spinal cord protection, but additional safeguards are warranted, including cerebrospinal fluid drainage and, when indicated, distal perfusion. For AA procedures that require resection of a significant portion of the descending aorta, we routinely monitor somatosensory-evoked potentials (SSEPs) and motor-evoked potentials (MEPs), which may provide superior monitoring of anterior cord integrity.24,25 Intercostal vessels are sacrificed gradually before instituting CPB. Each intercostal is provisionally clamped and sacrificed only if the MEPs and SSEPs remain unchanged for more than 10 minutes.26,27 MEP and SSEP monitoring is continued until the patient exits the operating room, to confirm the return and stability of signals. Mean arterial pressure is maintained at 80 to 100 mm Hg, or possibly higher if the patient has chronic, severe hypertension. Postoperatively, hourly clinical assessment of lower extremity function is performed for 72 hours. Any deterioration must be rapidly addressed by increasing the blood pressure and withdrawing cerebrospinal fluid (CSF) to decrease intrathecal pressure. These maneuvers to increase spinal cord perfusion pressure have proved successful in reversing late-onset paraparesis.27

Control of Hemorrhage

Most current aortic surgery is carried out using antifibrinolytic agents to inhibit bleeding. We routinely use epsilon-aminocaproic acid, but others have reported that tranexamic acid is as effective. Isovolumic hemodilution, with reinfusion of autologous whole blood following CPB and thromboelastography-guided blood product administration, has greatly reduced transfusion requirements.28 However, HCA exceeding 30 minutes or CPB exceeding 3 hours often requires factor replacement. Occasionally, particularly in reoperative or acute dissection cases, mediastinal packing and delayed closure may be required to control bleeding. We have experienced no mediastinal infections with this strategy. For persistent, low volume root hemorrhage that is expected to stop with normalization of hemostasis, a Cabrol fistula can be created in the superior mediastinum to shunt shed blood into the right atrium29 this maneuver may be lifesaving. Activated recombinant factor VIIa is indicated for patients with refractory, nonsurgical postoperative hemorrhage.30

Use of Glue

Surgeons have enthusiastically used gelatin resorcinol formaldehyde (GRF) and other biologic glues, predominantly for strengthening aortic tissue after acute type A dissection. Recently, however, there has been concern that the formaldehyde component of the GRF glue may cause tissue necrosis of the aortic wall, leading to late redissection and pseudoaneurysm formation.31,32 Alternatively, Bioglue (CryoLife, Inc., Kennesaw, GA), composed of bovine serum albumin and glutaraldehyde, has been used to strengthen friable tissues and also to seal suture lines, particularly in acute aortic dissection.33 Here too, however, evidence warrants caution, as tissue necrosis, as well as intraluminal aspiration and embolization, have been reported.34 In most scenarios we find glue unnecessary.

Treatment of Infected Grafts and Mycotic Aneurysms

Our initial strategy is to administer specific, intravenous antibiotics, when the organism is known, or broad spectrum for several days before operation. At surgery, the entire infected aneurysm or graft is removed and replaced. We have successfully used prosthetic grafts for this purpose, but many prefer cryopreserved homografts in this setting.16,35,36 Often the infecting organism can be cultured from the specimen. Intravenous antibiotics are continued for at least 6 weeks, and if a suitable oral agent can be found, therapy is extended for an additional 3 to 6 months.

If graft replacement must be performed in a frankly purulent operating field, the chest may be left open. The mediastinum is “washed out” after 24 to 48 hours and pectoralis or omental flaps may be brought into the wound and wrapped around the implanted prosthetic graft. A vacuum-assisted closure (VAC) dressing is applied and the mediastinum may be closed when signs of sepsis have resolved healthy granulation is present. C-reactive protein is a useful biochemical marker to help guide the length of antibiotic therapy and determine resolution of inflammation.17

Hypothermic Circulatory Arrest

Historical and Theoretical Considerations

Some of the earliest cardiac procedures were performed using HCA and in the 1960s, isolated case reports described the use of HCA in repair of AA aneurysms.37 Successful experience using HCA for correction of complex congenital heart lesions in infants, as advocated by Barratt-Boyes and associates,38 prompted renewed interest in its use in adults with aneurysms of the AA. The first series of such cases was reported by Griepp and associates,39 which promoted wide acceptance of the efficacy of HCA in protecting the brain in adult AA surgery. With experience, limitations of HCA were described, especially concerning the adequacy of cerebral protection during extended periods of HCA. More recently, strategies using HCA and SCP have been described, combining benefits of both techniques.

Enthusiasm for the use of hypothermia to protect the brain during circulatory arrest began with a series of investigations in adult dogs that documented profound inhibition of cerebral metabolism with lowering of brain temperature.40 Based on hypothermic versus normothermic metabolic rates, Michenfelder and Milde postulated that complete cerebral circulatory arrest for 30 minutes at 18°C would not result in permanent neurologic injury and subsequent experiments indicated that HCA for as long as 60 minutes should be safe.41 However, investigations in puppies42 and piglets43 showed that hypothermia suppresses cerebral metabolism less than that Michenfelder predicted. In puppies, cerebral metabolic rate at 18°C is reduced to only 40% of control levels, and HCA for 60 minutes at 18°C results in detectable early behavioral dysfunction and quantitative EEG changes.42,44 More prolonged HCA at 20°C in young piglets produces unequivocal behavioral sequelae and histologic evidence of cerebral damage.45

Experimental evidence indicates that the period of recovery following HCA is also critical. HCA, even for short intervals, engenders severe cerebral vasoconstriction that may last for hours. During this period, cerebral metabolism is maintained by increased oxygen extraction and thus is particularly vulnerable to hypoxic insult.44,46,47 High intracranial pressure also correlates with delayed neurologic recovery and subsequent cerebral histopathologic abnormalities. Oxygen saturation data also imply that cold reperfusion enhances cerebral blood flow for several hours postoperatively.

There are two basic mechanisms that lead to ischemic cerebral injury during operations on the thoracic aorta. Stroke, the first type of injury, has received the most attention, mainly because of its devastating consequences.48 These ischemic infarcts, detectable by conventional imaging techniques, result from embolic events, and are thought to be independent of the method of brain protection.49 The second type of injury results from focal or global ischemia, because of interrupted or inadequate flow, giving rise to the clinical syndrome temporary neurologic dysfunction (TND),49 which is characterized by varying degrees of obtundation, confusion, agitation, or transient parkinsonism. It is now generally accepted that TND is a direct consequence of inadequate cerebral protection and therefore related to the method of protection used.50,51

The incidence of TND in 200 adults who underwent HCA during thoracic aortic surgery was 19%, correlating significantly with age and duration of HCA. In this study, HCA averaged 47 minutes in patients with TND, and 33 minutes in those without TND. HCA duration did not correlate with mortality or permanent neurologic injury, which was usually focal, and was significantly more frequent in older patients and those with obvious atheromatous debris in the arch or descending aorta.49,50,52

Sensitive neuropsychologic testing showed that HCA exceeding 25 minutes and advanced age predicted poor performance in examinations of memory and fine motor function.53 Patients with impaired neurocognitive function several weeks postoperatively were significantly more likely to have manifested TND immediately postoperatively. Based on these findings, HCA exceeding 25 minutes must be considered a risk factor for long-term, albeit perhaps subtle, deficits in cognitive function. Impairment of memory may be related to injury of the hippocampus, which is particularly sensitive to ischemic injury because of its high metabolic rate.54

Past projections of the theoretical safe duration of HCA, based on rates of oxygen consumption at various brain temperatures, are now considered to have been misleading. The relationship between temperature and the cerebral metabolic rate for oxygen (CMRO₂) can be expressed as the temperature coefficient Q₁₀, which reflects the rate of reduction in the metabolism for a 10°C interval.55 The reduction of CMRO₂ with temperature is substantially more modest than that reported originally. In one experimental study, 39% of baseline CMRO₂ was still present at 18°C, a temperature previously thought to be safe for prolonged periods of clinical HCA; quantitative electroencephalography (EEG) showed significant slow-wave activity at 18°C, whereas EEG silence was present at 13 and 8°C.41

McCullough and associates55 recalculated Q₁₀ for the adult human brain based on direct measurements of CMRO₂ during HCA. These data predict that the safe period of arrest is about 30 minutes at 15°C and 40 minutes at 10°C, after which cerebral cellular anoxia occurs. These experimental findings correlate with ample clinical pediatric experience indicating that arrest times greater than 40 minutes portend poor neurodevelopmental outcomes.56 These observations support the use of truly profound hypothermia for circulatory arrest to achieve maximum cerebral metabolic suppression, particularly if arrest time will exceed 30 minutes. Intracranial temperatures should be protected from rising during HCA by packing the head in ice.43,44,46,47,57,58

Use of Corticosteroids

High-dose methylprednisolone, given 2 and 8 hours before CPB, reduces the change in cerebrovascular resistance and improves cerebral blood flow, cerebral arteriovenous oxygen difference, and oxygen metabolism following deep HCA, and may serve as a neuroprotective agent.59 Additionally, in 4-week-old piglets, pretreatment with corticosteroids 4 hours before CPB—compared with steroids in the CPB prime—reduced total body edema and cerebral vascular leakage, with improved immunohistochemical indices of neuroprotection.60 The beneficial effect of corticosteroid pretreatment derives from alterations in de novo protein synthesis at the mRNA level61 and inhibition of adhesion molecule expression in the endothelial cells, which impacts the trafficking of leukocytes into the injured areas.62 Other benefits of methylprednisolone given 8 hours before CPB and HCA are improved pulmonary compliance and alveolar-arterial gradient, and decreased pulmonary vascular resistance.63 Consistently, benefits are more apparent when steroids are given several hours before the institution of CPB.

Clinical Implementation

Because brain temperature primarily determines the safety of HCA, it must be measured accurately. Clinically available sites for measurement include: tympanic membrane, jugular venous bulb, nasopharyngeal, esophageal, bladder, and rectal. In our practice, we routinely monitor two different measurement sites to guide various phases of cooling and rewarming.

Throughout the duration of cardiopulmonary bypass, we follow arterial perfusate temperature, which best reflects the temperature that the brain is exposed to.

During cooling, esophageal or tympanic membrane temperature is used to reflect intracranial temperature and is monitored to guide the initiation of arrest. Based on clinical and laboratory studies,45,46,58 we cool for a minimum of 30 to 40 minutes, to an esophageal temperature of 15 to 18°C, with the perfusate lowered to 10°C. The head is packed in ice to prevent rewarming during HCA. Because continuing oxygen extraction reflects ongoing cerebral metabolic activity, we also monitor jugular venous saturation, using a target O₂ saturation of greater than 95% to indicate adequate cerebral cooling and metabolic suppression.

During rewarming, we primarily monitor the perfusate and bladder temperatures. The perfusate is kept at a gradient of no more than 10°C above the esophageal or tympanic membrane temperature, which reduces the likelihood that oxygen demand will exceed oxygen supply during the interval of inappropriate cerebral vasoconstriction after HCA.44,46,47,64 Avoiding high perfusate temperatures is also essential21 and we never allow it to exceed 37°C. The bladder temperature, which is raised to around 32–34°C, reflects total body or “core” temperature and lags considerably behind changes in the other temperature measurements during cooling and rewarming. Using the bladder temperature to guide rewarming helps to ensure uniform rewarming and prevent dangerous rebound hypothermia after CPB.

Following CPB, achieving hemostasis and maintaining normal hemodynamics are also important, since the vulnerable period of cerebral recovery, during which increased oxygen extraction is relied on to support adequate cerebral metabolism, may extend up to 8 hours postoperatively.

Selective Cerebral Perfusion

Historical and Theoretical Considerations

DeBakey reported the earliest attempts to repair AA aneurysms,65 in which a complicated technique of normothermic SCP was used, involving several pumps and bilateral cannulation of the subclavian and carotid arteries. Difficulty controlling pressure and flow to uniformly perfuse these separate vascular beds, as well as high operative mortality, led to early abandonment of this technique. However, SCP was revisited in the late 1980s, as mounting evidence indicated that HCA was not safe for the long durations required for repairing complex and extensive aneurysms. It was recognized that combining SCP with hypothermia permitted lower flow rates, while affording better cerebral protection than HCA alone or HCA plus RCP.66,67

Bachet and associates described perfusing the innominate and left carotid arteries with 6 to 12°C blood (flow 250 to 350 cc/min), which he termed “cold cerebroplegia.” Mortality for 54 AA cases was 3%, with only one severe neurologic injury and two transient focal lesions.68 Matsuda and associates69 used SCP at 16 to 20°C in 34 AA cases, with 9% mortality, 3% stroke, and 5% TND. His technique required a two-pump system and cannulation of the brachiocephalic and left carotid arteries; bilateral temporal artery and continuous internal jugular venous saturation were monitored and, importantly, the results demonstrated that hypothermic CPB did not carry a higher risk of coagulopathy.

Kazui first described his approach to SCP in 1986.70 Between 1990 and 1999, 220 patients underwent total arch replacement with SCP and open distal anastomosis, with 12.7% in-hospital mortality and 3.3% permanent neurologic dysfunction. Multivariate analysis showed in-hospital mortality was determined by renal failure, long CPB time, and shock; permanent neurologic deficit was associated with old cerebrovascular accident and long CPB duration.71 Perfusing two arteries with flows of 10 cc/kg/min at 22°C—considered 50% of physiologic levels, based on experimental studies—SCP duration had no significant impact on outcome.72

In a multicenter study, Di Eusanio definitively demonstrated the efficacy of SCP in reducing temporary and permanent neurologic dysfunction. In 588 patients undergoing both partial and full AA replacement, the risks of permanent and temporary neurologic injury were 3.8 and 5.6%, respectively; overall mortality was 8.7%.73

Clot or atheroma in the aorta, which often develops at the origin of the brachiocephalic vessels, predisposes to stroke during AA surgery. Therefore, complete arch resection should reduce the rate of neurologic injury. Accordingly, in 50 recent AA resections,74 Kazui and associates reported 2% mortality; permanent neurologic injury occurred in 4%, and TND in 4% (adverse outcome 6%), with a history of cerebrovascular disease a risk factor for permanent neurologic dysfunction.

The Kazui technique (Fig. 52-2A–H) begins with systemic cooling to 22°C, followed by circulatory arrest and SCP (22°C) delivered via malleable cannulas (Fuji System, Tokyo) inserted into the innominate and left common carotid arteries (Fig. 52-2B). Newly designed malleable cannulas allow superior visibility and simultaneous pressure monitoring (personal communication). With the left subclavian artery clamped, a four-branch graft is anastomosed to the descending aorta (Fig. 52-2C) and lower- body perfusion is begun via a side branch (Fig. 52-2D). Next, the left subclavian is anastomosed and perfused (Fig. 52-2E) followed by construction of the proximal anastomosis (Fig. 52-2F). Finally, full perfusion is restored by anastomosing the innominate and left common carotid arteries to the remaining side branches (Fig. 52-2G,H). Importantly, this technique includes transsection of the brachiocephalic vessels distal to their origins, precluding embolization of debris, and completely excluding the arch, which often contains friable atheromatous lesions.

Extensive aneurysmal disease, involving the ascending, arch, and descending aorta, can be resected in a single stage or may be approached by performing a two-stage procedure, wherein an elephant trunk graft, placed in the descending aorta during arch replacement, is used to simplify a subsequent procedure, performed via a left thoracotomy. In both approaches, SCP affords cerebral protection while permitting unhurried reconstruction of aortic continuity.

Rokkas and Kouchoukos75 described a single-stage reconstruction, the “arch first” technique, performed via bilateral anterior thoracotomies. This technique employs an interval of HCA followed by SCP while aortic continuity is restored. In 46 “arch first” procedures, the hospital mortality was 6.5%, with no permanent neurologic event and 13% TND.76 In 12 cases, HCA was minimized by administering unilateral SCP via the right axillary artery, averaging only 8.8 minutes.77

Unilateral administration of SCP has also been reported. For example, Kucuker and associates78 reported on 181 patients who underwent ascending and hemiarch replacement (90 patients) or total arch replacement (91 patients) with SCP delivered via the right brachial artery; hospital mortality was 6.6%, with 2.2% permanent strokes. The patients were cooled to 26°C and with the innominate, left common carotid, and occasionally the left subclavian artery clamped, arch replacement was performed with flow decreased to 8 to 10 cc/kg/min. The mean SCP duration was 36 ± 27 minutes (range 17 to 80 minutes). Contralateral cerebral flow was monitored by transcranial Doppler of the left middle cerebral artery. In the rare case of inadequate left hemispheric perfusion, an additional catheter was placed into the left common carotid artery. In this study, no mention was made of TND, but in a separate cohort of patients, neurocognitive testing revealed no postoperative deficits.79

Although contralateral perfusion was not problematic in these studies, a certain level of caution is prudent based on anatomic studies. Merkkola and colleagues found insufficient collateral circulation (<0.5 mm) through the circle of Willis in 14% of autopsy specimens.80

Recent clinical series have confirmed the relative safety of SCP. Khaladj and associates81 reported 501 consecutive cases (181 emergent), using moderate systemic hypothermia (25°C) and 14°C SCP administered via the innominate and left carotid arteries, maintaining perfusion pressure between 40 and 60 mm Hg and flows of 400 to 650 cc/min. The overall mortality was 11.6%, with 9.6% strokes and 13.4% TND. Permanent stroke risk increased with renal insufficiency and prolonged operative times, and TND risk increased with increased circulatory arrest time, emergency status, and concomitant coronary artery disease.

A small, randomized study by Kamiya and associates9 addressed a widespread concern that cannulation of the brachiocephalic arteries for SCP may cause cerebral embolization. High-intensity transient signals (HITS), indicative of microembolization—from sources such as gaseous microemboli, atherosclerotic debris, lipid microemboli, and blood-platelet aggregates—were quantified by transcranial Doppler monitoring in patients undergoing circulatory arrest with and without SCP. Only 0.6% of HITS were recorded during SCP, with most occurring during the interval between aortic cross-clamp removal and the termination of CPB. Thus, in this small subset of patients, SCP did not increase the risk of cerebral microembolization.

Using antegrade SCP for cerebral protection, many surgeons are performing arch surgery with moderate hypothermia (20 to 28°C). However, caution needs to be exercised at these temperatures, because end organs are more vulnerable to ischemia. To limit lower-body ischemia, thoracoabdominal perfusion during antegrade SCP has been recommended—via the femoral artery while clamping the proximal descending aorta, or with antegrade perfusion via an endoluminal balloon cannula in the descending aorta or via a sidearm graft branch of an arch graft.

Nonetheless, with precautions to prevent end-organ ischemia, a “global warming” trend has emerged, as surgeons have investigated ways to minimize or eliminate HCA. For example, 305 patients in Osaka, Japan underwent total arch replacement with SCP, combining right axillary and left common carotid perfusion.82 Perfusate temperature was progressively increased from 20 to 28°C. The duration of SCP was 150.1 minutes, with 60.9 minutes of circulatory arrest to the lower body. Operative mortality was 2.3%, with 1.6% permanent neurologic injury. Preoperative cerebral dysfunction was a risk factor for TND, which occurred in 6.6%. The strategy for patients with prior stroke included: higher CPB perfusion pressures (>60 mm Hg), more profound hypothermia (20 to 22°C), and higher SCP flows. In 67 aortic arch repairs at 28°C, the left subclavian artery was also selectively perfused, to increase collateral spinal cord blood flow during lower-body ischemia, and SCP flows were increased to 19 cc/kg/min to maintain arterial pressure at 60 mm Hg. Despite warmer SCP, outcomes remained consistent, with 6% mortality, 6% stroke, 1.5% TND, and no paraplegia. Another series of 120 acute type A aortic dissections had SCP administered via the right subclavian artery at 30°C, with snared brachiocephalic vessels,83 flow at 1320 cc/min, a perfusion pressure of 75 mm Hg, and average cerebral perfusion time 25 ± 12 minutes: 30-day mortality was 5%, stroke rate 4.2%, and TND rate 2.5%.

Although these and similar studies have yielded good clinical outcomes, there is no consensus regarding the optimal temperature for SCP and adopting warmer perfusion techniques during circulatory arrest should be approached cautiously. Experimental studies in a porcine model by Khaladj and associates84 indicate that the optimum temperature for SCP is no higher than 20°C, which resulted in lower intracranial pressures and earlier return of EEG activity than SCP at 30°C. Particularly noteworthy was evidence that although SCP provides good cerebral protection, the margin of safety for the spinal cord is thin. Our laboratory studies suggest that SCP at 10 to 15°C after HCA provides better cerebral protection than higher temperatures and clinically we use SCP at about 15°C.85

The duration of safe lower-body ischemia at 28°C is still under investigation, with evidence that 60 minutes may be the limit. If extended periods of circulatory arrest are anticipated, a method for lower-body protection should be utilized, such as femoral artery perfusion, aortic balloon occlusion with perfusion, antegrade perfusion through a sidearm graft, or deeper hypothermia. For example, 11 patients from a series of 252 ascending and arch repairs with moderately hypothermic SCP (25 to 28°C) had lower-body ischemic times greater than 60 minutes, and 2 (18%) developed paraplegia.86 In a porcine model, Etz et al. demonstrated that during 90 minutes of SCP at 28°C there is little or no spinal cord blood flow in the segment T4 to T13, resulting in a 40% spinal cord injury rate. Moreover, following SCP the lower spinal cord also lacked a normal hyperemic response, suggesting diminished vascular reactivity and localized edema. Histologic studies showed significant ischemic damage in the lower cord, even in animals that recovered clinically, suggesting that unappreciated spinal cord injury may be occurring even at shorter durations of lower-body circulatory arrest.

Clinical Implementation

In the current era, cerebral injury during AA reconstruction is most often related to embolization.112–114 Often, the arch and the origins of the brachiocephalic vessels contain friable, atheromatous debris, and the risk of embolizing this material can be minimized by using a brief period of HCA to transect the brachiocephalic vessels distal to their origins, completely excluding the diseased area. Then, during SCP, the arch repair can proceed in an unhurried fashion. Laboratory studies have shown that a short period of HCA does not compromise the superior cerebral protection provided by SCP.87

Our approach then is as follows. During a brief period of HCA, the individual brachiocephalic arteries are dissected free and sequentially anastomosed to a ready-made trifurcated graft, beginning either with the left subclavian or the innominate artery. The trifurcated graft is clamped, and SCP is instituted via the axillary artery (see Fig. 52-6D,E later in the chapter). Occasionally, when the left subclavian artery is displaced laterally and cephalad, a preoperative left subclavian to left carotid bypass is performed and a bifurcated graft is used to perfuse the left common carotid and innominate arteries (Fig. 52-3). Alternatively, a graft may be anastomosed to the left axillary artery and tunneled via the second ICS into the mediastinum. Hypothermic SCP is administered via the right axillary artery, typically requiring flows of 600 to 1000 cc/min to maintain mean pressures of 40 to 60 mm Hg, and the systemic perfusate temperature is allowed to drift upward. At the end of the arch reconstruction, the proximal end of the trifurcated graft is anastomosed to the ascending aortic graft. Using such strategies as axillary artery cannulation88,89 and grafting of individual brachiocephalic vessels during HCA,74,77,90,91 followed by SCP of the brachiocephalic grafts, lengthy periods of circulatory arrest are no longer necessary.

Retrograde Cerebral Perfusion

The early 1990s saw widespread enthusiasm for RCP92 based on the limitations of HCA, the success of retrograde cardioplegia, and isolated encouraging reports regarding the efficacy of RCP in treating massive air embolism.93 Purported mechanisms whereby RCP accomplishes neuroprotection include: (1) flushing embolic material from the cerebral circulation94 (2) providing cerebral flow sufficient to support cerebral metabolism95 and (3) maintaining cerebral hypothermia.96 There is, however, evidence that RCP may worsen neurologic outcome by inducing cerebral edema.97

Although initial laboratory and clinical reports regarding RCP were encouraging, many of the early studies used historical controls and short durations of RCP—well within the safe limits for HCA alone. Also, studies, in several animal species, demonstrated no flow to the brain during RCP.98–100 In other experimental studies, the most effective conditions for retrograde flow—including clamping inferior vena cava and high venous perfusion pressures—resulted in fluid sequestration, significant cerebral edema, and mild cerebral histopathology, sequelae observable even after relatively short intervals of RCP.94 Studies in our laboratory, measuring cerebral blood flow by collecting AA return and quantifying microspheres trapped in the brain, demonstrated that too little capillary flow occurs during RCP to confer metabolic benefit, even with inferior vena cava occlusion or during deep hypothermia.101 Similarly, directly visualizing cerebral capillaries with intravital microscopy showed that RCP does not provide adequate cerebral capillary blood flow to prevent ischemia but may induce brain edema.97 A cadaver study provided an anatomical explanation for poor retrograde flow, as functionally competent valves, demonstrated in the proximal internal jugular vein, obstruct direct retrograde intracranial venous flow, causing unbalanced and unreliable brain perfusion.102 However, a recent animal study showed that RCP may be helpful under some conditions, as intermittent pressure augmentation during moderate hypothermic RCP efficiently dilated the cerebral vessels, allowing an adequate blood supply without brain injury, and provided neuroprotection equivalent to antegrade SCP.103

The evidence from clinical studies is harder to interpret. Some studies show that RCP duration predicts mortality92,104 but others do not.105,106 Clinical studies comparing HCA+RCP and HCA alone have also yielded mixed results; some showed mortality rates comparable to other cerebral protection methods,107 and others showed reduced mortality rates with RCP.108–110 In three studies that included patients with SCP, HCA+RCP patients had similar mortality rates.111–113

In our own clinical studies,50,114 we have been unable to demonstrate any benefit of RCP. In a recent clinical study,50 we could not show a decrease in the incidence of stroke with RCP, perhaps because of a greater prevalence of patients with clot or atheroma in the RCP group, but arguably because RCP is not effective in preventing stroke. Mortality was higher in the RCP group, and TND was higher with RCP than with SCP. Furthermore, RCP resulted in no reduction of TND compared with HCA alone, reinforcing the notion that RCP probably has no nutritive value for brain tissue. As mentioned, our laboratory data suggest that RCP, especially at high pressures, although successful in removing some emboli, may aggravate cerebral injury.94 Clinically, this effect is not easy to demonstrate but may help account for our repeated observation that neurologic recovery is delayed in patients treated with RCP. Recently, we studied neuropsychologic dysfunction after RCP and found that RCP probably had a negative impact on cognitive outcome.115 Other investigators believe that neurocognitive dysfunction depends on the duration of RCP; if RCP duration is less than 60 minutes, recovery is comparable to that after CABG, whereas prolonged RCP is associated with neurocognitive impairment.116

In general, based on laboratory studies,96 we believe that the major benefit of RCP stems from continued cerebral cooling by venoarterial and venovenous anastomoses, which is especially helpful if systemic cooling is not as thorough or prolonged as it should be. Clinically, we no longer use RCP, feeling that its benefits derive not from providing nutritive support but from aiding in cerebral cooling and helping to prevent rewarming during HCA. However, we believe that it is safer to prevent rewarming by thorough initial cooling and packing the head in ice.

Clinical Implementation

Although we do not routinely use RCP for cerebral protection, many surgeons do administer RCP briefly following HCA in patients who have a high risk of embolization to help flush debris from the cerebral circulation.

RCP, which is always employed in conjunction HCA, by perfusing blood into either one or both venae cavae at a flow rate to maintain pressures of 15 to 20 mm Hg in the superior vena cava. Cardiac distention is avoided by choking both venae cavae. Given the rich network of collaterals between the superior vena cava and inferior vena cava, it probably makes no difference whether inflow is into one, the other, or both. When whole-body retrograde perfusion is carried out, the initial flow rate is usually 800 to 1000 cc/min, but once the venous capacitance vessels have been filled, flows of 100 to 500 cc/min are usually sufficient to maintain superior vena caval pressures at 15 to 20 mm Hg.

Hybrid Aortic Arch Repair

Endograft technology has permitted combining traditional open procedures with endovascular grafting, so-called hybrid procedures. Initially, stent grafts were deployed in the descending aorta for aneurysms involving the distal arch, or in lieu of an open stage II elephant trunk procedure. As experience accumulated, two problems attending aortic arch endografting became evident. First, there is often insufficient undilated aorta distal to the brachiocephalic vessels to seat the proximal portion of a stent graft. Second, the arch is often severely diseased and endograft procedures, which entail negotiating the arch with stiff wires and large-bore catheters, carry a risk of embolic stroke. In fact, experience showed that the more proximally an endograft was deployed, the higher was the risk of embolic stroke.117

Debranching Procedures

The technique of covering the origin of one or more brachiocephalic vessels with an endograft, generally in concert with bypassing or transposing them, addressed both problems by extending the proximal landing zone and minimizing the risk of atheroembolization. These debranching procedures118 involve transposing some or all of the brachiocephalic arteries to the ascending aorta. Initially performed on hypothermic CPB, debranching operations are now commonly done off pump, and permit endografting that partially or even completely excludes the aortic arch. The endograft may be introduced retrograde, via the common femoral artery, or antegrade, generally via a sidearm graft, variously configured to allow proximal access. Antegrade deployment offers the advantage of avoiding diseased and/or stenotic aortoiliac vessels. Debranching procedures presented many anatomical variations for endografting. The classification of landing zones described by Mitchell and associates (Fig. 52-4) allowed meaningful comparisons of different hybrid arch series.119 For comparisons of traditional total aortic arch repairs with current endograft-and-debranching procedures, only patients with zone 0 deployment constitute an equivalent match.

The Left Subclavian Artery

If the left subclavian artery is not accessible in the mediastinum, options for covering the subclavian origin with an endograft include: no revascularization; preemptive transposition or bypass of the left subclavian artery using the left common carotid artery; and left axillary artery bypass, wherein an axillary graft is tunneled into the chest and anastomosed centrally, often with subsequent coil embolization of the proximal left subclavian artery to prevent a type II endoleak.

Branched Grafts

Several branched graft techniques have been described for debranching. Canaud reported six cases with proximal endograft placement in zone 0, wherein debranching was achieved with a single 10-mm graft; end-to-side anastomoses were constructed to the brachiocephalic trunk and left common carotid artery and an end-to-end anastomosis was made to the left subclavian artery.120 Early postoperative complications included transient paraplegia, transient cerebral ischemia, cardiac tamponade, and a retrograde type A aortic dissection, successfully treated; there was no mortality at 30 days. With retrograde deployment in five patients, Chan placed endografts that occluded all the supra-aortic branches, revascularizing the innominate and left common carotid arteries using a bifurcated graft (14 × 7 × 7 mm)121 the left subclavian artery was revascularized only in cases of left vertebral dominance, left arm dialysis dependence, or a patent left internal mammary graft. Technical success was 100%, no neurologic complications, but two patients required reoperation for tamponade. Szeto and associates reported eight hybrid arch repairs performed via median sternotomy, with retrograde endograft deployment.122 Debranching was achieved using a patch giving off three branches, fashioned from a commercially available four-branched arch graft; the patch was anastomosed to the proximal ascending aorta using CPB, moderate hypothermia, and aortic cross-clamping. Two patients suffered TND and required long-term tracheostomy, and one died of myocardial infarction. Finally, Hughes published a series of 28 arch aneurysms, wherein 12 patients underwent total arch debranching using a custom-designed graft (Vascutek USA, Ann Arbor, MI), with limbs to allow transposition of the left common carotid and innominate arteries and antegrade stent-graft deployment.123 The left subclavian origin was covered in all patients, and two underwent left subclavian to common carotid bypass during the same procedure. Outcomes were excellent, with no deaths or strokes and one case of delayed paraparesis.

Although debranching has permitted stent grafting into zone 0, the stability of the proximal landing zone remains a focus of concern with current stent-graft technology. In the Hughes study,123 two type I endoleaks occurred, despite seating the proximal graft directly into a Dacron graft. To minimize this complication, the authors recommend oversizing the endograft by 20% and creating a 4-cm zone of coaptation when stenting into prosthetic grafts. Antona described a novel technique for ensuring stable proximal fixation, involving banding the aorta with a separate vascular graft to create a nonexpandable, cylindrical landing zone.124 The graft is opened longitudinally and wrapped around the aorta to create a 3- to 4-cm zone with an outer diameter of 32 mm. A radiopaque wire is used to mark its proximal and distal extent, facilitating subsequent retrograde endografting. In light of these experiences, most agree that future endograft systems must provide increased flexibility to follow the curvature of the aortic arch, yet achieve strong fixation to prevent endoleaks and secondary migration.

Aortic arch reconstruction requires different approaches, techniques, and operative strategies, depending on the arch pathology and the involvement of the proximal and distal aorta. To illustrate, we describe seven different situations and our approach to arch reconstruction in each of these cases.

Case 1: Bentall Procedure and Hemiarch Replacement

This is an elderly patient with stenosis of a severely calcified bicuspid aortic valve and an aneurysm extending from the root to the proximal arch (Fig. 52-5A).

Via a median sternotomy, using right atrial and right axillary artery cannulation, CPB and core cooling are initiated. The ascending aorta cross-clamped and transected, using antegrade and retrograde cold blood cardioplegia, supplemented by topical cooling, for myocardial protection. The perfusate temperature is maintained at 10°C until the esophageal temperature reaches 20°C and is maintained at that level while the Bentall procedure is performed. Coronary buttons, 1 to 1.5 cm in diameter, are fashioned and mobilized and the remaining proximal aorta is excised. A composite valved-conduit, constructed by suturing a bioprosthetic valve into a tube graft, is implanted, using interrupted pledgeted sutures. Using an ophthalmic electrocautery, an opening in the conduit for the left button is made, carefully situated to avoid stretching, twisting, or kinking of the left main coronary artery; the button is anastomosed using 4-0 or 5-0 polypropylene incorporating a thin strip of Teflon to reinforce the button.125

The perfusate temperature is dropped to 8 to 10°C during anastomosis of the left coronary button and, when the jugular oxygen saturation is above 95% and the esophageal temperature is 18°C, HCA is begun and the cross-clamp is removed, with the head packed in ice and the patient placed in Trendelenburg position. The distal ascending aorta and proximal arch are excised, leaving a beveled aortic cuff extending from the base of the innominate artery on the right to 1 cm proximal to the ligamentum arteriosum and the recurrent laryngeal nerve on the left. The composite graft is beveled and anastomosed to the aorta with 3-0 polypropylene suture material (Fig. 52-5B). A secure, hemostatic anastomosis is constructed by “sandwiching” the aorta between the graft, carefully invaginated within the aortic lumen, and a 1-cm cuff of Teflon felt, incorporated outside the aorta.22 Perfusing through the axillary artery, air is flushed from the aorta and cold perfusion is continued for several minutes before rewarming (Fig. 52-5C). A gradient of 10°C or less between the perfusate temperature and esophageal temperature is maintained throughout rewarming. With the heart filled and the aorta pressurized, the appropriate location for the right coronary button is marked, after which the distal graft is cross-clamped. The right coronary button is implanted and, before tightening the suture line, the heart is de-aired. The duration of HCA is usually less than 20 minutes and 50 to 60 minutes of core warming are generally necessary to raise the esophageal temperature to 35°C and the bladder temperature to greater than 32°C, at which point the patient is weaned from CPB.

Case 2: Total Aortic Arch Replacement for Atherosclerotic and Calcified Aneurysms

The arch and the origins of the supra-aortic vessels often contain friable atheromatous material and our trifurcated graft technique for total arch replacement (Fig. 52-6A–L) is designed to minimize manipulation of these segments before excluding them from the cerebral circulation, thereby reducing the risk of embolization; the technique minimizes cerebral ischemia by permitting antegrade SCP during arch reconstruction.126,127

A median sternotomy incision is extended superiorly along the medial border of the left sternocleidomastoid muscle. The recurrent laryngeal nerve is preserved as the AA and its branches are exposed. A no-touch technique of dissection is used—the patient is dissected away from the aneurysm.

CPB is initiated, using the right axillary artery and the right atrium, with the perfusate temperature lowered to 10°C (Fig. 52-6B). TEE is used to confirm flow in the arch and monitor for dissection or malperfusion. If the ascending aorta is calcified or severely atherosclerotic, it is not cross-clamped. Just before circulatory arrest, with the heart vented, 60 mEq of potassium chloride is added to the perfusate over 2 minutes to induce diastolic cardiac arrest. Alternatively, the heart is arrested with retrograde blood cardioplegia. If a proximal repair is required, it may be performed at this point, while core cooling proceeds (Fig. 52-6C).

Even in patients with severe atherosclerotic disease of the AA, the arch vessels just beyond their origins are usually spared, making this location ideal for subsequent anastomoses. A trifurcated graft is chosen corresponding to the sizes of the innominate, left carotid, and left subclavian arteries. The patient is placed in Trendelenburg position to prevent air trapping and the head is packed in ice to prevent rewarming during HCA. When the esophageal temperature reaches 18°C, and jugular bulb oxygen saturation is greater than 95%, HCA is initiated and the arterial perfusion line is clamped to prevent back filling of air during HCA.

The innominate artery is transected just distal to its origin, or at the level where atherosclerosis is minimal, and using 5-0 polypropylene, is anastomosed to the large limb of the trifurcated graft, which is generally trimmed close to its origin. The common carotid and the left subclavian artery anastomoses are constructed in a similar fashion and each anastomosis takes 6 to 10 minutes. Reversing the order of anastomoses may provide better access to the left subclavian artery in some patients (Fig. 52-6D). After de-airing, the proximal portion of the trifurcation graft is clamped, restoring perfusion to the head and upper extremities (Fig. 52-6E). Perfusion pressures are maintained at 40 to 60 mm Hg, requiring flows between 600 and 1000 cc/min. The perfusate temperature is allowed to drift upward to 16 to 20°C at the end of HCA, but active rewarming is not initiated until AA reconstruction is complete.

Alternative strategies can shorten HCA. For example, if the left subclavian and innominate artery anastomoses are completed first, then SCP can be infused (at a lower flow rate: 400 to 600 cc/min) via the axillary artery while the left carotid, gently clamped, is anastomosed. This maneuver can reduce HCA time to less than 20 minutes (Fig. 52-6K), but with favorable anatomy, HCA can be avoided completely by gently clamping all the brachiocephalic arteries, and implanting them stepwise onto the trifurcated graft (Fig. 52-6L).

It is important for postoperative pulmonary toilet to preserve recurrent laryngeal nerve function. When reconstructing the arch, a suitable cuff of aortic tissue is maintained to preserve the recurrent laryngeal nerve. Aneurysmal disease involving the distal arch can be treated in two stages, avoiding potential laryngeal nerve injury, by constructing an elephant trunk18,90,128 at a point in the distal ascending aorta or arch where the caliber permits. In this case, the transected brachiocephalic vessel origins are oversewn with 3-0 or 4-0 polypropylene; the “trunk anastomosis” is constructed with running 3-0 polypropylene, reinforced with a strip of Teflon felt (Fig. 52-6F). The proximal end of the elephant trunk graft is used to complete whatever root or ascending repair was undertaken; if a graft-to-graft anastomoses is required, it is constructed with 2-0 or 3-0 polypropylene, as these never heal and beveling both grafts helps to maintain the proper curvature (Fig. 52-6G,H). Next, the reconstructed aorta is distended to identify the appropriate site to attach the trifurcated graft, at which point an elliptical opening is made with ophthalmic electrocautery (Fig. 52-6I). This anastomosis is constructed with the trifurcated graft clamped, so that cerebral and upper extremity perfusion is uninterrupted. On completing this anastomosis, removing the clamp on the trifurcate graft restores full myocardial and systemic perfusion (Fig. 52-6J).

Case 3: Total Arch Replacement with an Aberrant Left Vertebral Artery

On occasion, the left vertebral artery (LVA) originates directly from the AA, posing a small challenge during arch reconstruction with a branched graft.129 This anomaly can be recognized on CT angiography and should prompt a duplex ultrasound evaluation of the right vertebral artery (RVA) to ensure patency and antegrade flow. With a patent, normally sized RVA, the LVA can be temporarily occluded during SCP and reimplanted during rewarming. Three options have been used (Fig. 52-7): direct reimplantation of the LVA into the left common carotid artery, attachment of a portion of reverse saphenous vein to the vertebral artery, and anastomosis to the arch graft or the left subclavian limb of the trifurcated graft. This last technique is essential if any question of the integrity of the RVA exists. A very small LVA (<2 mm) with a patent RVA may be ligated. Follow-up imaging studies have confirmed continued patency.

Case 4: Thoracosternotomy for Arch Reconstruction

Dr. Kouchoukos described a one-stage, repair, via a bilateral anterior thoracotomy, for patients with arch and proximal descending aortic disease, the “arch first” technique (Fig. 52-8A–G).76,130 This approach provides excellent exposure of the transverse AA and proximal descending thoracic aorta, but requires sacrificing both internal mammary arteries. Brachiocephalic artery reconstruction can be achieved with a Carrel patch or a branched graft technique.

The heart and great vessels are exposed via bilateral thoracotomies in the fourth interspace and transverse sternotomy. The right atrium is cannulated and the circuit organized so that arterial return can be directed to a side arm graft sewn to the axillary artery (see Fig. 52-8A) or to a cannula in the right common femoral artery. CPB and profound systemic cooling are initiated, with arterial return directed via the axillary artery, and the heart is vented via the right superior pulmonary vein or LV apex. During cooling the brachiocephalic arteries are exposed, carefully preserving the recurrent laryngeal and phrenic nerves. The distal limit for resecting the descending aorta is identified and mobilized circumferentially.

At 18°C, HCA is initiated, the brachiocephalic arteries are transected and the distal aorta is clamped. The brachiocephalic arteries, backflushed by slowly perfusing the right axillary artery, are sequentially clamped, beginning with the left subclavian artery (Fig. 52-8B). SCP is administered via the right axillary artery and, with flow increased to 10 to 15 cc/kg/min at 20°C, lower-body perfusion is established via the femoral arterial line. The aneurysm is opened, preserving a cuff of aortic tissue containing the recurrent laryngeal nerve. Using a four-branched graft, the brachiocephalic arteries are reimplanted, beginning with the left subclavian artery and proceeding proximally (Fig. 52-8C,D); at this point axillary perfusion can be used to flush the arch vessels (Fig. 52-8E) and, by clamping the graft proximally and distally, to administer SCP (Fig. 52-8F). Lower-body perfusion is discontinued and, with the distal aortic clamp removed, an open distal anastomosis is created. Increasing pump flows, the clamp is withdrawn from the distal arch graft and the patient is rewarmed, flowing antegrade via the sidearm graft. A proximal anastomosis is then performed to complete the arch reconstruction (Fig. 52-8G).131

Case 5: Arch Replacement Following a Previous Bentall Procedure for Extensive Thoracic Aortic Aneurysmal Disease

AA replacement after previous ascending aortic surgery can be challenging, but a simple approach can facilitate repair and avoid pitfalls. The arch is exposed through the previous sternotomy and the brachiocephalic vessels are dissected free. The previous graft is not extensively dissected, as it risks injury to the pulmonary artery. The patient is cooled on CPB, established via the right atrium and right axillary artery, and the LV is vented. During HCA, a trifurcated graft is anastomosed to the brachiocephalic vessels, as previously described, followed by administering SCP. The arch vessel stumps are oversewn with pledgeted 3-0 polypropylene.

An elephant trunk is constructed proximal to the origin of the innominate artery, leaving a long “trunk” extending into the proximal descending aorta. If the reoperation is for residual chronic aortic dissection, the elephant trunk should not be longer than the distal fenestration, to allow perfusion of the true and false lumens. However, if the false lumen is partially filled with thrombus, the elephant trunk should be directed into the true lumen to avoid embolization, with no fenestration performed. The proximal anastomosis is constructed to the previous Bentall graft with 2-0 or 3-0 polypropylene. The trifurcated graft is then attached to an elliptical opening made in the right lateral side of the old Bentall graft (Fig. 52-9). The arch remains pressurized pending a second-stage repair, performed using either an open surgical or endograft approach. Using this technique, we have reduced our morbidity and mortality to values comparable to first-time arch replacement.

Case 6: Descending Thoracic Aortic Aneurysm Involving the Distal Arch

Descending thoracic aortic aneurysms often involve the distal AA (Fig. 52-10A). If not severely calcified or atherosclerotic, in which case we prefer a two-stage reconstruction to isolate the cerebral circulation and reduce the risk of embolic stroke, we approach these with the following technique.

A left thoracotomy is performed in the fifth or sixth intercostal space and, if necessary, extended inferiorly across the costochondral plate to improve exposure. The descending aorta is gradually mobilized, serially clamping and sacrificing intercostal arteries, if SSEPs and MEPs do not change132 care is taken not to manipulate the arch adjacent to the left subclavian artery. The right atrium is generally cannulated via the left common femoral vein, but the main pulmonary artery can also be used for venous inflow. The left common femoral artery is cannulated for arterial return. Perfusion is begun gradually to avoid flow shifts in the aorta that might dislodge atheromatous debris and during CPB manipulating the aorta is minimized, as dislodged debris will be carried retrograde toward the arch vessels and coronary arteries. Alternatively, CPB with antegrade flow can be established by perfusing through an 8- or 10-mm PTFE ring-reinforced graft sewn to the right axillary artery, an arrangement that also permits SCP. During cooling, and particularly after ventricular fibrillation has occurred, any indication of LV distention by TEE or pulmonary artery pressure monitoring warrants LV venting via the LV apex or left atrium. Core cooling is continued until the esophageal temperature has decreased to 18°C and the jugular venous saturation has reached 95%, which generally takes 30 to 40 minutes. At this point, 60 mEq of KCL is slowly added to the pump perfusate, inducing diastolic cardiac arrest, and, with the LV vent clamped, HCA is initiated.

The descending aorta is opened, creating a beveled cuff under the arch, while preserving the recurrent laryngeal nerve. A “reverse hemiarch” anastomosis is created, using a sidearm graft (Fig. 52-10B). The brachiocephalic vessels are gently aspirated and, to facilitate de-airing and removal of debris, the cardioplegia line is attached to the LV vent and cold blood is infused at approximately 400 cc/min to flush out the LV, ascending aorta and arch. Alternatively, continuous perfusion of the lower body will maintain some collateral flow into the brachiocephalic vessels and assist in removal of air and particulate debris. At this point, perfusion is restored to the brachiocephalic and coronary arteries by flowing through the sidearm graft, with the main graft and subclavian artery clamped.

The distal anastomosis is constructed to the descending aorta after a brief period of femoral perfusion to flush debris. The clamp on the graft is removed, restoring flow to the entire body. During rewarming, an 8- or 10-mm graft is sewn to the left subclavian artery and anastomosed to the descending graft (Fig. 52-10C,D).

SSEP and MEP monitoring is continued to the conclusion of the operation and arterial pressures are maintained in the high normal range. The evoked potentials gradually return, but initially are below baseline because of systemic hypothermia. Depending on the extent of resection, an intrathecal catheter, placed preoperatively, is used to drain CSF in order to maintain the CSF pressure below 12 mm Hg for the first 48 to 72 hours.

Case 7: Hybrid Aortic Arch Repair for Distal Arch Aneurysms

Although aortic arch debranching can be performed off pump, it is safer to use CPB for the difficult anatomies encountered in many patients. Moreover, the off-pump approach requires placing a side-biting clamp on the pulsatile ascending aorta, posing a risk for intimal injury and subsequent aortic dissection.

On CPB, using a side-biting clamp, the main portion of a trifurcated graft is anastomosed to the ascending aorta with 4-0 polypropylene (Fig. 52-11A). The left subclavian artery, clamped, divided, and either stapled or oversewn proximally, is anastomosed to a limb of the trifurcated graft with 5-0 polypropylene, after which perfusion is restored. Similarly, the left common carotid and innominate arteries are attached to the remaining limbs. Temporary occlusion of each brachiocephalic artery is well tolerated, with no significant reduction in cerebral oximetry. If antegrade endograft deployment is planned, the trifurcated graft is modified by adding a proximal sidearm graft for access (see Fig. 52-11A). Difficult subclavian artery anatomy can be avoided by performing a preoperative carotid-subclavian bypass (Fig. 52-11B) or an intraoperative extra-anatomic bypass to the left axillary artery, tunneled through the first or second intercostal space (Fig. 52-11C).

Recent series of total AA replacements compare favorably with our results. Safi and associates133 reported 5.1% 30-day mortality in 117 stage I elephant trunk reconstructions, with 6.8% adverse outcomes. Interestingly, 37% of patients did not return for second-stage repair, and 30.2% died from distal aneurysm rupture during short-term follow-up. Schepens and associates,134 in 100 consecutive stage I elephant trunk reconstructions from 1984 to 2001, reported 8% mortality, 12% adverse outcomes, and 2% TND; the majority of these patients received unilateral or bilateral antegrade SCP for cerebral protection. Coselli and associates,135 in a series of 227 patients with AA surgery, reported 6% early and 9% late mortality, with 3% stroke, attributing a relatively low incidence of reduction in neurologic injury to using RCP during HCA in more than 50% of cases. LeMaire and associates reported impressive results for 55 total arch replacements using the trifurcated graft; despite 60% reoperations, there were no in-hospital mortalities, with one 30-day death, and three perioperative CVAs, one of which was transient.136 Kazui and associates,74 in their contemporary series of 50 patients, also achieved outstanding results: 2% mortality, 6% adverse outcome, and 4% TND. CPB duration was the only univariate risk factor for TND and a history of CVA was correlated with permanent neurologic dysfunction. Di Eusanio and associates,73 published a multicenter study using antegrade SCP for total arch replacement in 352 patients, wherein there was 8.7% in-hospital mortality, 3.8% permanent strokes, 5.6% TND, and 12.5% adverse outcome. Independent predictors of adverse outcomes included urgent operation, recent stroke, tamponade, unplanned coronary revascularization, and pump time. Finally, Numata and associates,137 using right axillary perfusion and a separate cannula in the left common carotid artery for 120 arch replacements, achieved excellent results: 5.8% mortality and 0.8% permanent stroke rate, with 5.8% TND.

From our prospectively compiled database, we identified 206 consecutive patients (125 males, 81 females) between September 1999 and September 2009, who underwent elective arch replacement with a trifurcated graft, using a brief interval of HCA (30 minutes [17 to 48]), followed by hypothermic SCP (69 minutes [21 to 125]; 15.8°C [12.0 to 22.1]), administered via direct axillary artery cannulation. The mean age was 67 (20 to 87 years), the most frequent etiology (37.3%) was chronic dissection, and 32.0% had atherosclerosis. Known risk factors included chronic obstructive pulmonary disease (13.6%), insulin-dependent diabetes (4.9%), hemodialysis (4.9%), and reoperations (44.2%). Potential risk factors for postoperative neurologic injury include a history of transient ischemic attack (2.4%) and preoperative stroke (9.2%).

The mean maximum aortic diameter was 6.0 cm (4.0 to 12 cm). Isolated arch replacement was undertaken in 23.8%; concomitantly resected segments included the ascending aorta (49.5%), ascending aorta and aortic root (12.6%), and the descending aorta (3.9%). Concomitant procedures included elephant trunk procedures (92.2%) and CABG (25.7%).

Hospital mortality was 6.8%, with 10.1% adverse outcomes and 3.3% permanent strokes. Postoperative complications included prolonged (>48 hours) intubation (13.1%), TND (5.8%; not correlating with preoperative neurologic risk factors), reoperation for bleeding (5.3%), and temporary (4.4%) or permanent (1%) renal support. The median ICU stay was 3 days (1 to 108 days) and hospital stay was 11 days (4 to 108 days).

The two facets of neurologic protection—prevention of cerebral injury during global ischemia and avoidance of particulate atheroemboli—are not mutually exclusive and the overall neurologic protection strategy must be an integral part of the AA replacement technique. To this end, two surgical strategies have emerged to balance the neurologic risks: the four-branched graft technique73,138,139 and the trifurcated graft technique.91 As compared with the classic Carrell patch technique,39 both reduce HCA and use SCP.

Generally, AA aneurysms are localized manifestations of a diffuse aortic disease process and therefore monitoring unresected segments following aortic surgery is a sensible precaution. Accordingly, we offer our patients a follow-up program and maintain a prospective database of all aneurysm patients. Patients with small aneurysms are advised to have ongoing imaging at 1- to 2-year intervals, depending on the aneurysm's etiology, location, and rate of progression. Postoperative patients receive a baseline CT angiogram or MRA to assess the repair and provide a baseline for later comparison. If no portion of the unresected aorta exceeds 4 cm, the first reevaluation is scheduled for 1 year, but a significant residual dissection or aneurysmal dilatation merits follow-up in 6 months.

Survival at 1 year is 74% in our trifurcated graft series, reflecting failure to return for a second stage, rupture before the second stage, and mortality from second stage. Among patients alive a 1 year, survival at 3 and 5 years is 94% and 78%.

Numerous publications confirm the importance of continued surveillance after AA surgery. Crawford and associates140 found that 70% of patients with AA operations had significant disease elsewhere in the aorta, Coselli and associates documented that 15% of 227 patients with AA repairs required additional surgery within 17 months,135 and Heinemann and associates141 reoperated on 24% of 82 patients with type A dissection over a 10-year period. Detter and associates,142 examining the long-term prognosis of aortic aneurysm in patients with and without Marfan's syndrome, found reoperations in 66.7% versus 10.7%; late mortality was 25% versus 14%, with 18% caused by redissection and recurrent aneurysm in the Marfan's group. In our follow-up of 162 patients post-repair of type A aortic dissection, 17% required reoperations: 23 distal and 4 proximal.143