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Acute aortic dissection is still the most common of all aortic catastrophes and is associated with significant morbidity and mortality. The natural history of acute type A aortic dissection has been reported as 1% per hour in the first 48 hours, or approximately 50% at 2 days, 75% at 2 weeks, and 90% at 1 year.
Early death may occur as a result of mal-perfusion syndromes (cerebrovascular, visceral, renal, or peripheral ischemia), cardiac complications (acute aortic insufficiency, coronary ischemia, cardiac tamponade), or free rupture. Because of poor outcomes from nonoperative management, urgent repair of acute type A aortic dissection is recommended.
Even with prompt diagnosis and immediate surgical intervention, poor outcomes are still expected. Although acute type A aortic dissection can be associated with a wide spectrum of complications, neurological injury remains one of the most devastating. The incidence of permanent neurological injury (stroke) during these repairs ranges from 1 to 11%, and is associated with increased early and late mortality.
Prolonged focal ischemia caused either by cerebral emboli or mal-perfusion is responsible for stroke. The specific etiology of TND is unclear, but most likely it is associated with subclinical micro-emboli or generalized cerebral mal-perfusion. In a study evaluating profound hypothermic circulatory arrest during transverse aortic arch repair, the incidence of TND was directly related to the duration of cerebral ischemia. This suggests cerebral mal-perfusion and suboptimal cerebral protection.
Since first being reported by Griepp, profound hypothermic circulatory arrest for cerebral protection has become widely used during complex aortic reconstructions.
For this reason, other cerebral protective strategies were used in conjunction with PHCA. These included retrograde cerebral perfusion and selective antegrade perfusion.
Rationale for RCP
Shortly after retrograde cerebral perfusion (RCP) was first described for proximal aortic repairs,
Surgical treatment of aneurysm or dissection involving the ascending aorta and aortic arch, utilizing circulatory arrest and retrograde cerebral perfusion.
it became a standard adjunct for cerebral protection during profound hypothermic circulatory arrest (PHCA) at many centers. Some researchers, ourselves included, have utilized RCP and observed enhanced survival and outcome.
The cited benefits of RCP include ease of establishment, uniform cooling of the brain, flushing of atheromatous and gaseous debris, and possible provision of nutrient flow to the cerebral circulation, although the reliability of this last advantage is debatable. Several studies have reported the metabolic benefits of RCP during PHCA in animals, but demonstrating these benefits in humans has been difficult.
Part of the problem in determining the usefulness of RCP is the difficulty in detecting reversed cerebral blood flow to the brain. Many groups have experimented with transcranial Doppler (TCD) ultrasound for the purpose of monitoring cerebral blood flow,
but inconsistencies in the identification and monitoring of cerebral blood flow have done little to clear up these uncertainties.
We recently adopted Power Motion-mode transcranial Doppler ultrasound (PM-TCD), invented by Moehring and Spencer, for monitoring middle cerebral artery blood flow during RCP.
Transcranial power M-mode Doppler displays flow intensity and direction over 5 cm of intracranial space simultaneously via a 33-sample gate. One of the advantages of this mode of insonation is that all flow signals that are obtainable along a given position and direction of the ultrasound beam may be displayed. Since PM-TCD enables easier location of acoustic windows when compared with a single gate spectral TCD,
we are able to monitor cerebral blood with greater sensitivity during RCP and throughout the course of the operative procedure. Other techniques of cerebral monitoring that we currently use include near infrared spectroscopy (NIRS), electroencephalography (EEG), and jugular venous pressure and oxygenation monitoring.
Using jugular bulb oxyhemoglobin saturation to guide onset of deep hypothermic circulatory arrest does not affect post-operative neuropsychological function.
Evaluation of the transverse arch during acute aortic dissection determines whether the entire (total) transverse aortic arch or just the proximal transverse (hemiarch) arch will be replaced. In general, we prefer to not replace the entire transverse arch in the setting of acute type A aortic dissection. As previously reported, replacement of the total transverse arch is associated with increased morbidity, e.g., bleeding, stroke, and decreased survival.
We do, however, replace the entire transverse arch when extensive hematoma, severe fragmentation of the intima, or free rupture of the transverse arch is present. In addition, we will replace the entire transverse arch in patients with significant aneurysmal enlargement (diameter greater than 5.0 cm) of the transverse arch or in patients with known connective tissue disorders like Marfan‘s syndrome. When transverse arch replacement is indicated, complete resection is performed with reattachment of the great vessels using an island patch. In patients with Marfan’s syndrome, we prefer to use the multi-branched woven polyester grafts and perform individual bypasses to the great vessels to exclude all native aorta. If enlargement of the proximal descending thoracic aorta is identified, then we perform the first stage “elephant trunk” procedure. We then replace the descending thoracic aorta using the elephant trunk, usually 4 to 6 weeks later. In most cases, we will perform replacement of the proximal transverse arch (or hemiarch) with either resection or primary repair of any transverse arch tears.
In this article, we illustrate our techniques of repair for acute type A aortic dissection. We will present both repair of the proximal transverse arch (hemiarch) and total arch, as well as our management of the aortic valve and aortic root. We will emphasize retrograde cerebral perfusion and the cerebral monitoring techniques used to verify cerebral blood flow.
Surgical Techniques
Anesthetic Management
Anesthetic induction utilizes fentanyl (10–15μg/kg), midazolam (0.05 mg/kg), and pancuronium (0.1 mg/kg). Aprotinin is administered as a one million-unit load followed by an infusion of 250,000 U/hr. Maintenance of anesthesia is achieved with continuous administration of isoflurane 0.5 to 1.0%and an oxygen/air mixture. Transesophageal echocardiography is used, and hemodynamics are controlled to achieve a cardiac index between 2.0 to 3.0 1/min/m2. Serial atrerial blook gas measurements are obtained, and the hematocrit is kept at greater than 24% while the patient is warmed and is allowed to drift to no less than 18% when the patient is cooled. Alpha stat management is used for acid base control throughout the procedure. All patients are monitored utilizing 5-lead electrocardiogram, peripheral pulse oximetry, end-tidal carbon dioxide (CO2) measurement, temperature probes (nasopharyngeal, bladder or rectal, and blood), arterial line placement, and pulmonary artery catheter.
Cardiopulmonary Bypass Circuit-Cooling Phase
After systematic anticoagulation, cardiopulmonary bypass is established by either right or left femoral artery cannulation depending on the patient’s pulse status. If no pulse is palpable, then axillary artery cannulation is performed. Because any arterial cannulation approach is susceptible to organ mal-perfusion at any time during the procedure, cerebral monitoring to verify cerebral blood flow becomes important. Venous cannulation is obtained via the superior vena cava and inferior vena cava or femoral vein. Snares are applied to both the inferior and superior vena cava for total CPB. Systemic cooling is initiated and the patient’s temperature is monitored using both nasopharyngeal and bladder temperature probes. We believe that nasopharyngeal temperature most closely approximates cerebral temperature.
Myocardial protection is achieved using continuous retrograde cold blood cardioplegia through the coronary sinus supplemented with direct antegrade coronary ostia infusion once the aorta is opened. A left ventricular sump is inserted through the right superior pulmonary vein. Both cell saver and pump suction are used for blood salvage.
Figure 1Power-M-mode Transcranial Doppler ultrasound is performed by a neuro-ultrasonographer or trained anesthesiologist (A). Shortly after induction, the patient’s head is fitted with a probe fixation head frame using a hands-free standard 2 MHz pulsed wave TCD transducer (Spencer Technologies, Seattle, WA) that is positioned on the temporal bone window for monitoring the middle cerebral artery blood flow velocity (cm/sec). The mean flow velocities and pulsatility indices (PI) are obtained using a single channel spectral display at assumed zero angle of insonation at the depths represented by a yellow line on the PM-TCD screen display. Bilateral middle cerebral artery blood flow velocities are monitored continuously. Any reduction in PM-TCD velocity less than 50% of baseline is reported to the operating surgeon. Patients are monitored using bilateral NIRS-INVOS (Somanetics, Troy, Michigan) and a 10-lead electroencephalogram (EEG) monitors cerebral function (B).
Figure 2Although any organ mal-perfusion can have devastating implications, this article will focus specifically on cerebral mal-perfusion. If cerebral mal-perfusion is observed, then operative maneuvers are performed to improve cerebral blood flow. In our experience, episodes of cerebral mal-perfusion have been identified in one of three time periods: at initiation of or early in cooling of cardiopulmonary bypass (from 30°C to 35°C), late in cooling during cardiopulmonary bypass (from 22°C to 30°C), and at the initiation of cardiopulmonary bypass with warming after completion of the distal reconstruction.
1. If cerebral mal-perfusion is identified at the initiation or early in CPB, then CPB is discontinued and an alternative site for arterial cannulation is established with either the contralateral femoral artery or axillary artery. Cerebral perfusion is then confirmed.
2. If cerebral mal-perfusion is identified late in the cooling phase, then an alternative arterial cannulation site can be established, but we prefer performing proximal aortic fenestration. During a brief period of circulatory arrest, the patient is placed in the Trendelenberg position; a longitudinal aortotomy is performed on the mid-ascending aorta; the dissecting membrane is fenestrated into to arch beyond the great vessels (A); an aortic cross-clamp is applied distal to the aortotomy on the ascending aorta; cardiopulmonary bypass is then reestablished (B). Cerebral monitoring confirms cerebral blood flow.
3. After completion of the distal aortic reconstruction and reestablishment of antegrade flow (the warming phase), cerebral mal-perfusion can be identified, especially when the transverse aortic graft is directly cannulated with the arterial cannula. We currently use the commercially available single side-arm branched grafts and have thus eliminated this problem.
Figure 3Once the EEG is isoelectric, which coincides with a nasopharyngeal temperature of 15° to 20°C, CPB is discontinued and circulation is arrested. Since our indicator for adequate cerebral cooling before arrest is isoelectric EEG and not time of cooling, rapid cooling can be performed (our average cooling time to isoelectric EEG is 22 minutes), thus reducing the overall cooling and warming periods. Longer cooling times may be required if discrepant nasopharyngeal (cerebral) and bladder (core) body temperatures exists. We do not cool below 12°C. Retrograde cerebral perfusion is initiated through the superior vena cava cannula using a centrifugal pump. Jugular venous pressure and RCP pressure are monitored separately. We initiate RCP of 500 mL/min and increase this pressure until reversal of middle cerebral artery blood flow is identified; this pressure is termed the “opening pressure.” Once reversal of MCA blood flow is identified, the RCP flow can usually be reduced, as guided by PM-TCD, from the opening pressure to a lower RCP pressure termed the “maintenance pressure” for the duration of circulatory arrest. Under profound hypothermic circulatory arrest, the ascending and transverse aortic arch are inspected. Then the ascending aorta is opened. The tear is characterized and its location is identified. If the tear is isolated to the ascending aorta or proximal transverse aortic arch, then replacement of the proximal transverse arch or hemiarch is performed. Those with a second limited tear located in the transverse arch can be repaired primarily using 4-0 pledgetted polypropylene sutures.
Figure 5We prefer to use the side-arm branched commercialized woven Dacron graft. This graft is cut in a beveled fashion to correspond to the size of the proximal transverse arch aorta. This is then sutured to the Dacron graft using a running 4-0 polypropylene suture. From the inside, the posterior wall of the suture line is then reinforced using multiple interrupted 4-0 pledgetted polypropylene sutures.
Figure 6After completion of the posterior row, the anterior layer is completed using the running 4-0 polypropylene suture. The anterior layer is then reinforced using multiple interrupted 4-0 pledgetted polypropylene sutures.
After completion of the distal anastomosis, RCP is discontinued and flow started via the femoral arterial cannula so as to flush any debris from the transverse arch. The side-arm branched graft is cannulated with a second arterial line that is secured and allowed to flow and flush. After adequate flush, an aortic cross-clamp is applied to the ascending/transverse graft and antegrade perfusion initiated. Perfusion through the femoral arterial cannula is discontinued. The patient is placed in a level position. After adequate hemostasis of the distal reconstruction is noted, the systemic warming is begun in the antegrade fashion.
Figure 7If the transverse arch is enlarged (greater than 5 cm in diameter) or if free rupture, extensive intimal disruption, or extensive arch hematoma is present, then we perform a formal total arch. Again the false lumens are obliterated by suturing the separated layers using a running 4-0 polypropylene sutures.
Figure 8The Dacron graft is sutured to the proximal descending thoracic aorta directly, or if slight enlargement of the proximal descending thoracic aorta is noted, an elephant trunk is performed. Each suture line is made using a running 4-0 polyproylene suture. This is re-enforced using multiple interrupted 4-0 pledgetted polypropylene sutures.
Figure 9For cases in which the descending thoracic aorta is enlarged after realignment of the aortic layers, then the elephant trunk procedure is performed. The brachiocephalic vessels are reattached as an island patch. If the patient has a history of Marfan’s syndrome or other connective tissue disorders, then bypasses to the brachiocephalic vessels are performed using the premanufactured multi-branched transverse arch grafts.
Figure 11(A) While systemic warming is performed, attention turns to the proximal reconstruction. All attempts are made to preserve the valve and the aortic root if possible. The ascending aorta is completely resected to the level of the sinotubular junction. We use 4-0 polypropylene stay sutures to realign the aortic wall layers.
Figure 11(B) Aortic valve resuspension is performed using interrupted horizontal mattressed 4-0 pledgetted polypropylene sutures at each commissure. In our experience, the aortic valve can be preserved in most patients. We will replace the aortic valve only if the valve leaflets are destroyed by the dissection or if significant native disease (calcifications) are present. In patients with bicuspid aortic valves, we will preserve the valve unless significant native disease (calcifications) is present. In patients with Marfan‘s syndrome, we can perform valve preserving aortic root replacement using the re-implantation technique, but we prefer to replace the aortic root including the valve, especially if the annulus is also enlarged in the setting of acute dissection.
Figure 11(C) After resuspension or replacement of the aortic valve, we inspect the aortic root. Aortic root reconstruction is performed by first evacuating any thrombus or fresh blood from between the layers of the root. This allows alignment of the aortic layers and evaluation of the aortic root. The size of the root is evaluated. The location and involvement of the coronary ostia are inspected and patency is determined by infusing cardioplegia into each ostia. If dissection involves the coronary ostia and primary repair cannot be performed, then coronary artery bypass is performed “blindly” to a distal point using an autogenous saphenous vein graft. The proximal coronary ostia is then oversewn using 4-0 pledgetted polypropylene sutures.
For aortic root reconstruction, the walls are aligned by placing a row of interlocking interrupted 4-0 pledgetted polypropylene sutures circumferentially at the level of the sinotubular junction. Multiple rows may be required depending on the nature of the tissues and extensiveness of the dissection. We feel that this technique for aortic root reconstruction is important for reducing retrograde dissection and rupture in the short term as well as aortic root enlargement in the long term.
After completion of the aortic root reconstruction, the graft is distended, cut to the appropriate length, and sutured to the sinotubular junction using a running 4-0 polypropylene suture. This again is reinforced using interrupted 4-0 pledgetted polypropylene sutures both inside on the posteriorly and on the outside anteriorly.
Figure 12The heart and graft are de-aired, and the aortic cross-clamp is removed, perfusing the heart. Warming is continued until the patient’s core body temperature reaches 36°C. Blood and nasopharyngeal temperature never exceeds 37°C. The patient is weaned from CPB, systemic anticoagulation is reversed, and the patient is decannulated.
Figure 13In most cases, the aortic root can be salvaged; however, if the native root is enlarged (greater than 5 cm in diameter) or destroyed with extensive disruption of the sinuses the aortic root is replaced. This is also the case if the patient has a history of a connective tissue disorder.
Figure 14Relationships of pump flow, pressure, and Power M-mode Transcranial Doppler (PMD-TCD) velocity during retrograde cerebral perfusion. 1. Cooling phase: relatively constant pump flow and systemic pressure; PMD-TCD velocity may decrease. 2. Circulatory arrest phase: Antegrade pump flow is discontinued; systemic pressure falls; PMD-TCD velocity disappears. Retrograde cerebral perfusion (RCP) begins with increasing pump flow and cerebral venous pressure. Once reversed, cerebral artery flow is identified with PMD-TCD; at the corresponding opening pressure, RCP pump flow is decreased still maintaining reversed cerebral blood flow at a maintenance pressure. 3. Warming phase: antegrade pump flow is reinitiated; systemic circulation is restarted. M2 = M2 branch of the middle cerebral artery; M1 = M1 branch of the middle cerebral artery.
In our series of 208 patients who presented with acute type A aortic dissection, the hospital mortality was 20.2% (42/208). Fifty-seven patients (27.4%) presented with hypotension (SBP <90 mm Hg or need for inotropic support), and forty-five of these patients (21.6%) presented with either free or contained rupture into the pericardial sac. In those who were not ruptured, the hospital mortality was 9.1%. The total arch was replaced in 11.8% of cases, aortic valve was replaced in 10.5% of cases, and the aortic root replaced in 9% of cases. Retrograde cerebral perfusion was used in 96.2% of cases.
Guided Cerebral Perfusion
We recently reported our results using PM-TCD to guide retrograde cerebral perfusion during repairs of the ascending and transverse aortic arch. In this study, we identified that an “opening” RCP pressure was required to identify reversal of blood flow in the middle cerebral arteries.
In addition, when using standard RCP flow and pressure (0.5 L/min and less than 25 mm Hg), reversal of MCA blood flow was identified in only 20% of cases, and 80% of cases required some modification of RCP flow. Similar to the above study, more recently, we examined the use of PM-TCD during repairs of acute type A aortic dissection. We found that 78.5% of patients required modification of RCP flow to identify reversal of MCA blood flow. In addition, the RCP pressures in this study were significantly higher than in the control group, 33.3 ± 7.1 versus 26.7 ± 10.6, P = 0.008. This higher pressure was the again the “opening” pressure required to identify reversal of MCA blood flow
The requirement of a higher opening pressure (as opposed to maintenance pressure) may be related to an increase in cerebral-venous resistance as a result of the conversion from antegrade to retrograde perfusion or the need to overcome competent venous valves.
At any rate, standard RCP flows and pressures (0.5 L/min and 25 mm Hg) may not be adequate to achieve reversed cerebral perfusion during RCP. When Tanoue and coworkers utilized TCD to identify cerebral blood flow during RCP, with RCP pressure limited to less than 20 mm Hg, they observed reversed cerebral blood flow in only 3 of 15 cases.
The standards for RCP pump flow and pressure were established early on, with most centers regulating RCP at a pump flow of 500 mL/min with care to avoid RCP pressures over 25 mm Hg.
Surgical treatment of aneurysm or dissection involving the ascending aorta and aortic arch, utilizing circulatory arrest and retrograde cerebral perfusion.
Although we did observe high opening RCP pressures, we did not observe PMD-TCD evidence of increased cerebral edema, which would have manifested as significantly different pulsatility indices and post bypass end-diastolic flow velocities.
In addition, clinical evidence supplied by physical examination or radiographic evaluation demonstrated no increased cerebral edema. A recent animal study that evaluated increased RCP pressures (34–40 mm Hg) reported amplified cerebral tissue perfusion, but no rise in tissue edema at higher RCP pressures.
Using data from cerebral circulation studies, it has been estimated that the amount of cerebral blood flow derived from RCP may range from 20% to 60% of antegrade cerebral blood flow during CPB.
The difference in cerebral blood flow is attributed to venous shunting during RCP. Although a significant amount of RCP flow may lead to venous shunting, it has been determined that the amount of RCP flow that reaches the cerebral circulation is directly dependent on the RCP pump flow.
In the past, we have used a conventional maximum flow rate of 500 mL/min in the RCP circuit and kept superior vena cava line pressure below 25 mm Hg. But without cerebral monitoring, it is unknown whether or not reversal of cerebral blood flow is achieved or the potential benefits of RCP maximized.
Not only is PM-TCD used for circulatory arrest phase to guide RCP flow, it is also used to maintain cerebral monitoring throughout the repair. Because mal-perfusion can occur at any phase during the repair of acute type A aortic dissection, PM-TCD can identify cerebral mal-perfusion providing the potential for correction. In our recent study using PM-TCD for monitoring during repair of acute type A aortic dissection, we were able to demonstrate a significant improvement in neurological outcome (temporary neurological dysfunction).
In addition to PM-TCD, 2-channel TCD monitoring and Near Infrared Spectroscopy (NIRS) have been used for cerebral monitoring during complex aortic repairs. The advantage of the multi-channel PM-TCD is the larger window for detection as compared with 2-channel TCD monitoring.
This allows for a higher sensitivity in the identification of cerebral blood flow. However, this technology is limited by its dependence on a skilled technician for the operation of the monitor. As with TCD in general, PMD-TCD is also limited by patient variables. The use of PMD-TCD assumes that an adequate temporal window is available. Near infrared spectroscopy has also been utilized for cerebral monitoring during repairs requiring PHCA.
Most of these studies report using NIRS to monitor cerebral oxygenation with no attempts to modify operative techniques if a decrease is noted. We are currently studying the significance of NIRS during PHCA.
Many controversies still remain with regards to the optimal technique for cerebral protection (retrograde cerebral perfusion versus selective antegrade cerebral perfusion) and optimal cannulation approach for the establishment of cardiopulmonary bypass (femoral, axillary, or direct aortic) during complex aortic repairs. Regardless of the approach or technique preferred, the use of cerebral monitoring (PM-TCD, NIRS, or EEG) to confirm and potentially guide cerebral perfusion during repairs of acute type A aortic dissection may improve outcomes.
Acknowledgments
We like to thank Charles C. Miller, III, PhD and Tricia Cramblet for the illustrations and Kirk Soodhalter for his editorial assistance.
Surgical treatment of aneurysm or dissection involving the ascending aorta and aortic arch, utilizing circulatory arrest and retrograde cerebral perfusion.
Using jugular bulb oxyhemoglobin saturation to guide onset of deep hypothermic circulatory arrest does not affect post-operative neuropsychological function.
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