Acute type A aortic dissection is impressively morbid. Fifty percent of patients suffering acute type A aortic dissection are dead within 48 hours if untreated.16 Data such as these suggests that acute type A dissection carries a "1% per hour" mortality for missed diagnoses. More contemporary data reveal a different prognosis such that medical management may be considered in certain high-risk groups. In one such study in octogenarians, type A dissection was managed medically in 28% of patients for various reasons with a 58% in-hospital mortality.8 Regardless, because of the extreme mortality with medical management, patients surviving acute type A aortic dissections must be aggressively diagnosed and treated with surgical intervention.
Initial Medical Management
The high morbidity of acute type A aortic dissection dictates that management should precede confirmation of diagnosis in highly suspicious cases. The initial patient encounter centers on making the diagnosis while identifying factors that require immediate treatment. The site of this initial evaluation and resuscitation is determined primarily by the hemodynamic stability of the patient. The unstable patient belongs in the operating room, whereas a more detailed diagnostic approach and subsequent management can be undertaken in stable patients. Therefore, the hypotensive patient, whether from hemorrhagic shock or tamponade, requires the aforementioned evaluation and resuscitation on transfer to the operating room. It is preferable to avoid procedures such as TEE or central line placement on an awake patient outside the operating room because hypertension resulting from patient discomfort may precipitate aortic rupture or propagation of dissection. However, as in any patient with potential aortic rupture, anesthetic induction remains dangerous in patients compensating for impaired preload, whether from pericardial fluid or hypovolemia. The operating room must be prepared for prompt decompressive pericardiotomy and/or initiation of cardiopulmonary bypass.
In the hemodynamically stable patient, blood pressure is measured in both arms and both legs. These dissections can propagate in either direction, but proximal propagation can quickly destabilize the situation. In general, the goals of hypertension management in acute aortic dissection, regardless of anatomy, are twofold.4 First, transmural aortic wall stress is diminished by decreasing the systolic blood pressure, which reduces the possibility of rupture. Second, shear stress on the aorta is decreased by minimizing the rate of rise of aortic pressure to decrease the likelihood of dissection propagation, so-called anti-impulse therapy. Specifically, the immediate goal for this situation remains to achieve a target systolic blood pressure between 90 and 110 mm Hg with a target heart rate of less than 60 beats per minute.
Pain control is important to reduce catecholamine release and decrease the risk of rupture. Therefore, therapy begins with pain control using narcotic analgesics. The drugs most commonly used for anti-impulse therapy are beta-blockers and peripheral vasodilators. In most cases, beta-blockers such as esmolol should be used first because adequate heart rate control may be difficult if the blood pressure is controlled by peripheral vasodilators first and because vasodilators may increase ventricular ejection and aortic shear stress if used unopposed. Short-acting beta-blockers should be titrated to a heart rate less than 60 beats per minute. After beta-blocker treatment has been initiated, vasodilators such as sodium nitroprusside are used for further blood pressure control. Sodium nitroprusside is a direct arterial vasodilator with a short onset and duration of action, which makes it ideal to rapidly achieve the target systolic blood pressure. Loading doses for esmolol and sodium nitroprusside should be avoided to prevent hypotension. Alternative beta-1 blocking drugs such as propranolol or metoprolol, and the combined alpha- and beta-blocker labetalol are appropriate in the subacute phase. Calcium channel blockers may be necessary to reduce systolic blood pressure in those patients with a contraindication to beta-blocker use. A commonly used alternative to nitroprusside is nicardipine. This is also a calcium channel-blocker devoid of any cardiac effects which is easily titrated to a goal blood pressure.
The goals of surgery in acute type A dissection are to prevent or treat an aortic catastrophe while restoring blood flow to the true lumen of the aorta. Aortic catastrophe includes aortic rupture into the pericardium or pleural space, dissection and occlusion of the coronary ostia, and progression to aortic valvular incompetence. The presence of ascending aortic involvement is therefore an indication for operative management in all but the highest-risk patients (Table 50-5). The difficulty arises in determining which patients are high risk and which additional factors should affect the management algorithm. Patient age, for example, is not regarded as an absolute contraindication to surgery. However, this factor should be considered given the relative worse outcomes of operative treatment for acute type A dissection for patients greater than 80 years of age. Neurologic status at the time of presentation can also affect the decision to operate. Although most agree that obtunded or comatose patients are unlikely to improve with surgical repair, complications such as stroke or paraplegia at the time of presentation are not contraindications to surgical correction. It must be acknowledged that dissection repair will most likely not improve neurologic condition, and may even make it worse. Neither the distal extent nor the thrombosis of the false lumen obviates the need for surgical repair because the risk of developing an aortic catastrophe remains. Similarly, patients with subacute type A dissection who present or are referred after 2 weeks of dissection onset require operation. Scholl et al demonstrated that these patients have avoided the early complications of dissection and may safely undergo elective operation rather than emergency repair.17
Table 50-5 Operative Indications for Acute and Chronic Type A and B Thoracic Aortic Dissection |Favorite Table|Download (.pdf)
Table 50-5 Operative Indications for Acute and Chronic Type A and B Thoracic Aortic Dissection
|Dissection type||Operative indication|
Failure of medical management (persistent or recurrent pain, medically uncontrolled hypertension)
Expanding aortic diameter
Impending or actual rupture
Impending or actual rupture
Symptoms related to dissection (congestive heart failure, angina, aortic regurgitation, stroke, pain)
Aneurysm ≥5.5 cm (type A), ≥6.5 cm (type B)
Aortic expansion >1 cm/yr
Anesthesia and Monitoring
Anesthesia used during the repair of aortic dissections is often narcotic based with inhalational agents for maintenance. Single-lumen endotracheal tubes are used for procedures performed through a median sternotomy, whereas double-lumen endotracheal tubes are useful but not mandatory for procedures performed through a left thoracotomy. Monitoring lines often include central venous access with a pulmonary artery catheter and one or more arterial pressure monitoring lines specific to the operation performed. Preparation must be made for all possibilities in these cases, most importantly for the possible need for hypothermic circulatory arrest. Arterial monitoring should be tailored to both the anatomy of the dissection and the method of cannulation. One or two radial arterial lines and at least one femoral line may be required to ensure adequate perfusion of the upper and lower body. All patients require a TEE probe. Core body temperature is monitored in the bladder using a Foley catheter and in the esophagus using a nasopharyngeal probe. A wide skin preparation to include the axillary and femoral arteries is essential to provide all possible cannulation options.
Neurologic monitoring is available, but its utility remains controversial even in elective cases. Advocates of both cerebral and spinal cord monitoring argue that these monitors are able to detect injury to neurons before irreversible cellular injury.18 Thus, this warning allows for detection of imminent injury and subsequent evasion of injury. Opponents argue that there is a significant learning curve and that the injury has already occurred once these monitors can identify ischemic neurologic changes. The optimal type of monitoring depends on the location of the dissection and the resultant details of required vascular control. Manipulation of the ascending aorta and arch can affect cerebral perfusion. In these cases, transcranial Doppler (TCD) or near-infrared spectroscopy (NIRS) have been used. Intraoperative TCD monitoring is used to identify malpositioned cannulas or document the need for adjustment of retrograde perfusion.19 Opponents of TCD argue difficulty with low baseline flow and poor signal in patients with thick temporal bones, which confuses interpretation of the results and the response to them. Continuous noninvasive NIRS can be used to monitor cerebral oxygenation, marker of cerebral blood flow. Although the role of NIRS in aortic dissection has not been elucidated, advocates extrapolate use from studies on carotid endarterectomy and coronary bypass. NIRS can be used for identification of regional oxygenation changes during the case, which may be particularly useful during normothermic periods of these cases.18 Somatosensory evoked potentials (SSEP) is argued to be useful in identifying neurologic injury ranging anywhere from the peripheral nerve to the brain. These studies may even identify ischemic cerebral injury during hypothermic circulatory arrest earlier than electroencephalography (EEG).20 SSEP can also be useful in the detection of spinal cord ischemia to identify crucial spinal cord vasculature requiring reimplantation. The use of SSEP at some centers has led to reduced intraoperative and postoperative paraplegia in retrospective studies.21 Neurologic monitoring remains a relatively new technology that is operator dependent, but probably is useful in experienced hands.
Open aortic dissection repair is commonly associated with significant blood loss caused by weak tissues and coagulopathy from bleeding or hypothermia. Strict blood conservation is an important aspect of the operation. At least one cell-saver device should be available. Packed red blood cells, platelets, and fresh-frozen plasma should be in the operating room at the start of the operation. Coagulopathy as a result of the preoperative status of the patient, cardiopulmonary bypass, and deep hypothermic circulatory arrest contribute to excessive blood loss. Antifibrinolytic drugs can be useful hemostatic adjuncts. Patients will often require transfusion of fresh-frozen plasma, platelets, and possibly cryoprecipitate. Fibrin glues and hemostatic materials such as Surgicel and Gelfoam are useful as systemic coagulopathy is corrected.
Cannulation for type A dissection repair requires thoughtful evaluation of the dissection anatomy while taking into consideration the extent of the repair to be undertaken. The crucial point is to provide arterial flow into the true lumen of the aorta with proof of sufficient end-organ perfusion, in particular as dynamic flaps may alter perfusion. Some flexibility regarding arterial access should be exercised. In certain situations, a patient may require multiple cannulation sites to adequately perfuse the entire body. Various options for cannulation exist, but the optimal choice of cannulation in aortic dissection requires tailoring to the combination of surgeon preference with dissection anatomy.
Venous cannulation remains relatively straightforward. Venous cannulation is obtained commonly through the right atrium using a two-stage venous cannula, whereas bicaval cannulation is used for certain cases in which retrograde cerebral perfusion is used during hypothermic circulatory arrest. A left ventricular vent is necessary in the setting of aortic valve incompetence and is easily placed through the right superior pulmonary vein or rarely through the left ventricular apex wall. Cardioplegia is administered in a retrograde fashion through a coronary sinus catheter with additional protection via direct cannulation of the undissected coronary ostia.
Arterial cannulation requires a much more thoughtful process. Historically, femoral cannulation was the site of choice for arterial cannulation for type A dissection. However, the optimal site of cannulation should be tailored based on the combined goals of surgery and the specific anatomy of the patient, with contingency plans for evidence of malperfusion.
The goals of surgery, in terms of distal extent of the repair, depend to a certain extent on surgeon's preference. Many surgeons feel that optimal repair should be limited to the ascending aorta. This scenario can be accomplished by cannulation at most sites with flow directed into the true lumen of the aorta. Femoral cannulation has been a traditional mainstay in dissection repair. The most favorable side of femoral cannulation has been debated in the past, but as long as there is perfusion into the true lumen, the side most likely does not matter. Reports from the University of Virginia, among others, have also shown that the dissection itself can be cannulated safely with echocardiographic guidance.22 This technique involves confirming access to the true lumen of the aorta with echocardiography of the descending aorta. Then, using the Seldinger technique, a percutaneous cannula can be properly positioned. Direct cannulation should be avoided through areas with evidence of hematoma. Proper perfusion of the true lumen must be confirmed with ultrasound or echocardiography. A potential salvage maneuver involves cannulation of the ventricular apex with advancement of the cannula though the aortic valve and into the true lumen of the aorta. This technique also requires confirmation of true lumen perfusion. Aortic cannulation of either the dissection area or the apex mandates cannulation of the graft after repair in most cases.
Other surgeons believe that resection of the maximal amount of abnormal aorta possible is ideal. Because this resection commonly involves the aortic arch, many choose to cannulate in a way that allows for antegrade cerebral perfusion. Although cannulation of the innominate and the left common carotid artery have been described, the most common cannulation site for arch cases has become right axillary cannulation.23 The right axillary artery provides direct access to the right carotid artery for selective antegrade perfusion. This can be done by sewing a graft to the artery or directly cannulating it. However, direct axillary cannulation appears to cause more morbidity than graft cannulation, including further dissection, brachial plexus injury, and limb ischemia. Axillary cannulation may be suboptimal in cases in which the axillary, right common carotid, or innominate artery are dissected. Similar techniques have been described in cannulation approaches to the innominate and left carotid arteries. Finally, the open aorta allows direct access to the lumen of the innominate and the left common carotid, which can be cannulated during hypothermic circulatory arrest for selective antegrade perfusion. No matter the preferred site of arterial cannulation, the surgeon must be cognizant of whole body perfusion. Patients that are not cooling properly or show other signs of malperfusion may require more than one arterial cannulation sites for cardiopulmonary bypass. Routine confirmation of blood flow in the carotids as well as the descending aorta can be critical to avoid malperfusion.
Type A dissection repair involving the arch disrupts blood flow to the brachiocephalic arteries during a period of circulatory arrest. Cerebral protection during that period is critical to neurologic outcome. Cerebral protection is optimized through deep hypothermia with or without potential neuroprotective adjuncts. Straight hypothermia during circulatory arrest was the first method used to perform operations on the aortic arch and remains an effective method for shorter procedures. Two alternative primary end points for cooling are employed: goal temperature or EEG silence.
The published temperature goals vary widely, namely anywhere from 14 to 32°C. The ischemic tolerance of the brain improves with colder temperatures. However, cooling to a temperature below 14°C can result in a form of nonischemic brain injury and is therefore not recommended. The neurologic protection from straight hypothermic circulatory arrest can be very good, especially for short ischemic times. Most data suggest that straight hypothermic circulatory arrest up to 20 minutes is safe. However, increased ischemic time is directly related to increased incidence of neurologic deficits.24 Proponents of straight hypothermic circulatory arrest have suggested in elective patients that longer times can be used safely without significant adverse cognitive outcomes but circulatory arrest should be limited to as short a time as possible.25
For these cases, temperature is being used as a proxy for metabolic function. Unfortunately, nasopharyngeal and tympanic temperature may be imperfect estimates of brain temperature. Moreover, temperature does not directly relate to neurologic activity. For these reasons, some groups use EEG silence to determine the appropriate point at which to discontinue cooling and perfusion. The patients are cooled until EEG silence is obtained. After 5 minutes at this temperature, the circulatory arrest period can be initiated, usually at a temperature between 15 and 22°C. Using this technique, the group from the University of Pennsylvania achieved EEG silence in 90% of patients after 45 minutes of cooling and had a postoperative stroke rate of less than 5%.26 As a result, in the absence of EEG monitoring, they cool for at least 45 minutes in almost all cases to optimize brain protection. Although EEG is attractive in theory, it is not always available when patients with dissections are taken to the operating room.
Continued cerebral perfusion during the period of circulatory arrest is an alternative technique for cerebral protection, especially for circulatory arrest times greater than 20 minutes. Cerebral blood flow may be delivered in either a retrograde or antegrade fashion. The technique for retrograde cerebral perfusion depends on the venous cannulation strategy. If bicaval cannulation is used, reversing flow through the superior vena caval cannula with a proximally placed tourniquet is simple and effective. Use of retrograde flow with dual-stage venous cannulation requires placement of a retrograde "coronary sinus" catheter into the superior vena cava through a pursestring suture. The superior vena cava is then occluded with an umbilical tape to direct flow toward the head. Retrograde cerebral perfusion has the added benefit of flushing atherosclerotic material and air from the brachiocephalic vessels. A flow rate necessary to produce a superior vena caval pressure of 15 to 25 mm Hg is considered optimal.
Selective antegrade cerebral perfusion has recently gained popularity. Once the aortic arch is open, the innominate artery and the left common carotid artery are encircled with vessel occluders and each lumen cannulated with a retrograde "coronary sinus" cannula. With the left subclavian artery occluded, flow rates are slowly increased to achieve perfusion pressures of 50 to 70 mm Hg at the desired circulatory arrest temperature. These cannulae are then removed just before completing the anastomosis of the brachiocephalic vessels to the vascular graft, at which time cardiopulmonary bypass may be reinstituted.
A few basic principles apply to all approaches. During cooling on cardiopulmonary bypass, a maximum temperature gradient between perfusate and patient of less than 10°C is ideal. The head is then packed in ice to maintain a low brain temperature. To ensure maximal protection, the goal temperature should be maintained for 5 minutes before initiation of hypothermic circulatory arrest. Similarly, the body should be reperfused for 5 minutes at the colder temperature before beginning the rewarming process. Rewarming too early can exacerbate neurologic injury. Rewarming proceeds without exceeding a 10°C perfusate-patient temperature gradient to at least 37°C as core body temperature often falls briefly after cessation of active warming and separation from cardiopulmonary bypass.
Pharmacologic adjuncts are believed by some to decrease metabolic rate with hopes of reducing injury. Although methylprednisolone continues to be used in these cases by many, barbiturate administration during cooling has fallen mostly out of favor. If used, methylprednisolone should be given early as the steroid effects require incorporation into the cell nucleus. Others give lidocaine and magnesium before the arrest period to stabilize the neuronal cell membrane. Furosemide and mannitol can be administered to initiate diuresis and promote free radical scavenging after circulatory arrest. The results of all these techniques are not fully substantiated yet.
The exposure for procedures performed on the ascending aorta and proximal arch is through a median sternotomy. This can be modified with supraclavicular, cervical, or trapdoor incisions to gain exposure to the brachiocephalic vessels or descending thoracic aorta. When dissecting the distal arch, it is important to identify and protect both the left vagus nerve with its recurrent branch and the left phrenic nerve. Replacement of the ascending aorta in type A dissections is best performed by an open distal anastomosis technique if the arch is involved (30%) or if arch involvement is unknown. The open distal anastomotic technique requires clamping the mid ascending aorta and producing cardiac arrest via administration of antegrade and/or retrograde cardioplegic solution. The dissected ascending aorta proximal to the clamp is then opened. Evaluation and surgical correction of the aortic valve is ideally performed at this time while systemic cooling continues. If the dissection does not involve the aortic root, the aorta is transected 5 to 10 mm distal to the sinotubular ridge. When the dissection involves the sinotubular ridge, the proximal aorta is reconstructed by reuniting the dissected aortic layers between one or two strips of Teflon felt using either 3-0 or 4-0 Prolene suture. Safi et al use a technique of interrupted pledgeted horizontal mattress sutures as compared with the felt sandwich technique.27 In their experience, this provides superior stabilization and decreases the potential for subsequent aortic stenosis. The University of Pennsylvania has described aortic reconstruction using felt as a neomedia giving a stable platform to sew the graft to otherwise friable tissue.26
Once the temperature reaches 18 to 20°C, perfusion is discontinued during a brief period of circulatory arrest. When using antegrade or retrograde cerebral perfusion, the selected perfusion is initiated at this time. The aortic clamp is released and the intima of the aortic arch is inspected and repaired accordingly (Fig. 50-13). If the intima is intact, the distal anastomosis is performed and the graft is cannulated, deaired, and clamped for resumption of cardiopulmonary bypass with systemic warming. If the intima of the arch is violated, then a hemiarch reconstruction is performed (Fig. 50-14). We have only rarely found it necessary to perform a complete arch resection for an acute dissection. If a complex aortic root procedure is required, it is often useful to repair the aortic root with one vascular graft and use a separate graft to create the distal aortic anastomosis. The two grafts are then measured, cut, and anastomosed to provide the correct length and orientation for aortic replacement.
The false lumen of the distal aorta is closed and the aortic wall is reconstructed with inside and outside felt strips.
(A) The type A dissection extends into the proximal aortic arch. (B) The distal dissected aortic wall is reconstructed with inside and outside felt strips to replace part of the arch and ascending aorta.
If the ascending aorta cannot be cross-clamped, the patient is cooled to 20°C with subsequent circulatory arrest. The distal aortic reconstruction is performed first in this circumstance, at which time the graft is cannulated and proximally clamped with resumption of cardiopulmonary bypass and systemic rewarming. Cannulation of the graft for antegrade systemic perfusion and rewarming is associated with improved neurologic outcomes compared with retrograde perfusion and should be performed whenever possible. Because a cross-clamp is not applied, the left ventricle must be decompressed once fibrillation starts during systemic cooling (approximately 20°C) to prevent distention and irreversible myocardial injury. Proximal ascending aortic repair is completed during the period of rewarming.
An alternative to the open distal technique is possible when the dissection is limited to the ascending aorta or the proximal arch away from the origin of the brachiocephalic vessels. Antegrade arterial perfusion is achieved through distal arch or right subclavian artery cannulation; retrograde perfusion via cannulation of a femoral artery has traditionally provided acceptable results. An aortic cross-clamp is applied tangentially just proximal to the innominate artery. The ascending aorta is resected to include the inferior aspect of the arch. The layers of the dissected aorta proximal to the clamp are then reunited if necessary and the ascending aorta replaced with an appropriately sized, beveled vascular graft. The proximal reconstruction and anastomosis may then be created and the entire procedure performed without requiring deep hypothermia and circulatory arrest.
Isolated dissection of the aortic arch is rare. Classified as a type A dissection, it requires resection of the arch at the site of intimal disruption and aortic replacement. Surgical management of the brachiocephalic vessels is determined by the integrity of the adjacent intima. If intact, the brachiocephalic vessels are reimplanted as a Carrel patch into a vascular graft after repair (Fig. 50-15). If the dissection involves individual vessels, each may require repair and reimplantation individually into the graft used for arch replacement (Fig. 50-16).
Brachiocephalic vessels can be reattached to an arch graft as a unit if the inner cylinder of origin of each vessel remains intact. (A) The arch vessels are excised as a unit from the superior surface of the dissected aortic arch. (B) The separated layers of the brachiocephalic patch are reunited using inner and outer felt strips and continuous suture. (C) A corresponding hole is cut in the aortic graft and the continuous brachiocephalic unit is sutured into place.
The brachiocephalic vessels are separated from the true lumen by the dissected false lumen (left panel). If individual brachiocephalic vessels are also damaged beyond repair, short interposition grafts are added to reconnect each artery to the aortic graft (right panel).
Aortic root dissection often fails to violate the intima of the coronary ostia. Repair of the ascending aorta at the sinotubular junction is therefore sufficient to reunite the aortic root layers and provide uninterrupted coronary blood flow. Minimal disruption of the coronary ostial intima should be repaired primarily with 5-0 or 6-0 Prolene suture. If, however, the ostium is circumferentially dissected and an aortic root replacement is necessary, an aortic button should be excised and the layers reunited with running 5-0 Prolene suture, glue, or both. Coronary buttons are then reimplanted into the vascular graft or to a separate 8-mm vascular graft as part of a Cabrol repair (Fig. 50-17). Aortocoronary bypass grafting is performed only when the coronary ostium is not reconstructable and as a last resort.
Illustration showing the attachment of the coronary ostia to the graft using the Cabrol technique. The ends of a 60-mm Dacron graft are sewn end to end to each coronary ostium. A side-to-side anastomosis is made between the intercoronary tube graft and the aortic graft.
Acute type A dissection is complicated by aortic valve insufficiency in up to 75% of patients. Fortunately, preservation of the native valve is successful nearly 85% of the time. The mechanism of aortic insufficiency in most cases is the loss of commissural support of the valve leaflets. This is repaired using pledgeted 4-0 Prolene sutures to reposition each of the commissures at the sinotubular ridge (Fig. 50-18). The dissected aortic root layers are then reunited using 3-0 Prolene suture and either one or two strips of Teflon felt to recreate the sinotubular junction and reform the sinuses of Valsalva. Aortic valve preservation must always be performed using intraoperative TEE to assess the valve postoperatively. No more than mild aortic insufficiency should be present. In addition to commissural resuspension, techniques exist to spare the aortic valve and replace the aortic root in acute type A dissection, but the experience is early and the number of patients few. This topic is covered in greater detail in the section on surgical techniques for chronic type A dissection.
Resuspension and preservation of the native aortic valve in a type A dissection. (A) The dissected layers are approximated at each commissure with double-pledgeted mattress sutures. (B) The aortic valve commissures are completely resuspended. (C) Thin felt strips (8- to 10-mm wide) are placed inside and outside from the circumference of the aorta. The coronary ostia are not compromised. (D) The aortic walls are sandwiched between the felt strips with a horizontal mattress. (E) A vascular graft is sutured to the reconstructed proximal aorta.
If the aortic valve cannot be spared, replacement of the ascending aorta and valve should be performed using a composite valve graft or homograft. The composite valve graft is implanted using horizontal mattress 2-0 Tycron sutures to encircle the annulus and to seat the valved conduit (Fig. 50-19). The previously excised and reconstituted coronary buttons are reimplanted into the vascular graft with running 5-0 Prolene suture (Fig. 50-20). The left coronary button is implanted first, at which time the graft is clamped and placed under pressure to define the proper orientation and position of the right coronary button. The aortic homograft is similarly implanted using horizontal mattress 2-0 Tycron sutures, except that a generous margin of aortic root below the coronary buttons is retained for a second hemostatic suture line of running 4-0 Prolene. This is an ideal solution for individuals who have a contraindication to anticoagulation or for young females. The Ross procedure (pulmonary autograft) is not applicable in those patients with connective tissue disorders and not recommended in acute dissection.
Everting 2-0 pledgeted mattress sutures are placed shoulder to shoulder around the aortic annulus to anchor a composite graft containing a St. Jude prosthesis.
The coronary ostia are attached to the graft by the button technique using continuous 5-0 polypropylene suture.
Invasive hemodynamic monitoring is used to ensure adequate end-organ perfusion with a target systolic blood pressure between 90 and 110 mm Hg. Early postoperative blood pressure control begins with adequate analgesia and sedation using narcotics and sedative/hypnotic agents. The patient should, however, be allowed to emerge from general anesthesia briefly for a gross neurologic examination. The patient is then sedated for a period to ensure continued hemodynamic stability and facilitate hemostasis. Coagulopathy is aggressively treated with blood products and antifibrinolytic agents as necessary, and by warming the patient. Hematocrit, platelet count, coagulation studies, and serum electrolytes are obtained and corrected as necessary. An ECG and chest radiograph are used to assess for abnormalities and to serve as baseline studies. A full physical exam, including complete peripheral vascular exam, is performed on arrival. Despite adequate repair of the dissection, perfusion of the false lumen may persist; therefore, malperfusion syndrome remains possible. If an abdominal malperfusion syndrome is suspected postoperatively, this should be aggressively evaluated with ultrasound and subsequent angiography if positive. A strong clinical suspicion is enough to warrant this evaluation given the consequences of failed recognition. The patient can be extubated once extubation criteria are met if the patient has been hemodynamically stable without excessive bleeding and the results of a neurologic exam are normal. Management is routine from that point forward.
Surviving the operation for acute dissection represents the beginning of a lifelong requirement for meticulous medical management and continued close observation. It has been estimated that replacement of the ascending aorta for type A dissection obliterates flow in the distal false lumen in fewer than 10% of patients. As a result, the natural history of repaired dissection may involve dilatation and potential rupture of the chronically dissected distal aorta. This was the reason for the late death in nearly 30% of DeBakey's original series in 1982 and is currently the leading cause of late death following surgical repair.28 Often a multidrug antihypertensive regimen including beta-blocking agents is required to maintain systolic blood pressure below 120 mm Hg. There are some data indicating that blood pressure control within a narrow range may alter the natural history of chronic dissection by diminishing the rate of aneurysmal dilatation. The long-term durability of the aortic valve after supracoronary reconstruction is quite good with freedom from aortic valve replacement of 80 to 90% at 10 years. Progressive aortic insufficiency of the native valve is possible and should be followed with TEE in some patients.
Follow-up diagnostic imaging is required to monitor aortic diameter in patients after repair. Spiral CT arteriogram and MRI are the imaging studies of choice. MRI and ultrasound are useful in patients with renal insufficiency and those requiring only imaging of the abdominal aorta. Echocardiography is useful for imaging the ascending aorta and provides additional information regarding the aortic valve. It is important to recognize the resolution limitations of each imaging modality and inherent imprecision of comparing different imaging modalities to evaluate changes. In general, measurements should be made at the same anatomical level with respect to reproducible anatomical structures (ie, the sinotubular ridge, proximal to the innominate or left subclavian arteries or at the diaphragmatic hiatus). It is important to recognize that the false lumen should be included in measurements of aortic diameter whether it is perfused or not. Three-dimensional reconstruction of spiral CT and MRI scans minimizes the error introduced by aortic eccentricity when comparing imaging studies and has simplified following this patient population. The current recommendations are to obtain a baseline study before hospital discharge and at 6-month intervals during the first year. If the aortic diameter remains unchanged at 1 year, studies are obtained yearly. Aortic enlargement of more than 0.5 cm within a 6-month period and greater eccentricity on comparison of 3D reconstruction images are high-risk changes for which the interval is decreased to 3 months if surgery is not indicated.
The operative mortality for repair of acute type A aortic dissection has fallen since DeBakey's original 40% mortality was reported in 1965. Improved ICU and floor care of these patients, earlier recognition of dissection through improved imaging modalities, development of hemostatic vascular graft material, more effective hemostatic agents, and improvements in the safety of cardiopulmonary bypass are likely responsible. In the last two decades, most centers consistently report an operative mortality for acute type A dissection of between 10 and 30%. The high early mortality in acute dissection parallels the number of patients who present profoundly hypotensive and in shock. The mode of death is stroke, myocardial ischemia/heart failure, aortic rupture, or malperfusion in most cases.
The International Registry of Acute Aortic Dissections (IRAD) recently reported on the results of 526 patients with acute type A aortic dissection who underwent surgical treatment in 18 large tertiary centers.29 Surgery in these patients included replacement of the ascending aorta in 92%, aortic root in 32%, partial arch in 23%, complete arch in 12%, and descending aorta in 4%. Overall in-hospital mortality was 25%; 31% for hemodynamically unstable patients and 17% for stable patients. Causes of death were aortic rupture (33%), neurologic complications (14%), visceral ischemia (12%), tamponade (3%), or nonspecified (42%).
Age is not an absolute contraindication to surgical treatment of type A aortic dissections. However, operative mortality increases with age. Retrospective series show that operative mortality increases from 20 to 30% for patients younger than 75 years of age to greater than 45 to 50% for those 80 years or older.30
The published results for long-term survival following surgically treated acute type A aortic dissection over the last decade is roughly 71 to 89% at 5 years and between 54 and 66% at 10 years.31–33 Survival for patients who are discharged alive from the hospital after surgical repair of type A aortic dissection carries a survival rate of 96% at 1 year and 91% at 3 years.34