Aortic dissection is the most common type of acute aortic syndrome. It occurs when a tear in the aortic intima allows blood to dissect into the wall of the aorta.1 Aortic dissection can result from abnormalities in underlying tissue structure, such as Marfan syndrome and Loeys-Dietz syndrome, or it can occur in previously asymptomatic patients with no known genetic aortopathy.2 Aortic dissections are commonly classified by their point of origin (Table 1). Stanford type A aortic dissections (TAADs), also known as DeBakey type I and type II dissections, arise within the ascending aorta or aortic arch. Stanford type B (DeBakey type III) dissections originate in the descending thoracic aorta distal to the left subclavian artery.3 While type B dissections are managed medically or with selective surgical intervention, TAADs are almost always considered a surgical emergency.4,5 A small subset of aortic dissections originate in the aortic arch and may extend distally into the descending thoracic aorta.6 Classification of these patients is controversial, but current evidence suggests survival with medical management that is comparable to patients with Stanford type B aortic dissection.7 Assuming no significant complications exist, such as malperfusion or progressive aortic expansion, patients with dissections of the aortic arch can be managed with antihypertensive therapy and close clinical follow-up.
The mortality rate of TAAD without intervention is approximately 1% per hour, with 50% of untreated patients dying within the first 3 days.8 With surgical intervention, overall in-hospital mortality ranges from 8% to 24%.9–13 Recently, the Penn classification was introduced to improve risk stratification of patients presenting for TAAD repair. The Penn system classifies TAADs based on ischemic symptoms at presentation, subdivided into localized ischemia (localized organ malperfusion or branch vessel occlusion) and generalized ischemia (circulatory collapse). This classification scheme has been demonstrated to predict mortality after TAAD repair.9,10,12,13
Given the urgent presentation, complex surgical management, and risk of mortality and organ dysfunction, TAAD remains a complex perioperative management challenge. The anesthesiology team should be aware of the presentation, hemodynamic management, surgical strategies, monitoring options, and potential complications. The following text discusses some of these challenges.
PRESENTATION AND PREOPERATIVE MANAGEMENT
Patients with TAAD typically present with acute chest and back pain, although they may present with syncope, abdominal pain, or symptoms of malperfusion of the viscera or limbs.14 Approximately 6% of patients present with heart failure or stroke with no other clinical symptoms. Diagnosis with computed tomography (CT) or transesophageal echocardiography (TEE) is most common, although transthoracic echocardiography (TTE), aortography, and magnetic resonance imaging can also be diagnostic.5,14 Artifacts on CT imaging may rarely result in false-positive diagnoses, primarily due to motion artifact in the ascending aorta or complicated aortic anatomy in patients with previous aortic procedures.15,16 In cases where the diagnosis may be uncertain (eg, remote hospital diagnosis and transfer with inadequate imaging), TEE should be used to confirm the diagnosis. Laboratory assessment of d-dimer, while nonspecific, has nearly 100% sensitivity for a TAAD, and a normal level almost certainly rules out aortic dissection.17,18
Preoperative assessment of the patient presenting for repair of a TAAD should focus on identifying issues that may complicate management or lead to morbidity or mortality before the initiation of cardiopulmonary bypass (CPB).19 Imaging should be reviewed to evaluate for leak from the aorta, which can proceed to frank rupture after sternotomy. Focused preoperative TTE may identify patients at increased risk of hemodynamic collapse after the induction of anesthesia. TTE can be used to evaluate volume status, as well as rule out pericardial effusion, acute aortic insufficiency (AI) ventricular dysfunction, or regional wall motion abnormalities from coronary dissection.20,21
Invasive blood pressure monitoring and large bore intravenous access should be obtained, and the patient should be initiated on antihypertensive and chronotropic therapy. β-Adrenergic blockers are typically first-line therapy for the control of hypertension, although vasodilator therapy or calcium channel blockade can be added to optimize control before operative intervention. Although clevidipine, nicardipine, sodium nitroprusside, and nitroglycerin can all be used as antihypertensives, current evidence suggests that clevidipine and nicardipine may be more effective in controlling blood pressure in patients undergoing cardiac surgery.22
Patients should be asked about a history of illicit drug use because approximately 10% of TAADs are caused by cocaine abuse.23,24 The use of β-adrenergic receptor antagonists in patients with acute cocaine intoxication is controversial because they may cause unopposed α-adrenergic activity and worsening of systemic hypertension.25 These patients may be best managed with a combination of benzodiazepines, calcium channel blockers, nitroglycerin, and α-2 agonists such as dexmedetomidine.25,26
Some patients with TAAD may present with signs of systemic hypoperfusion.27 In these patients, the suspected etiology of their shock should guide therapy before surgical intervention. Patients who are suspected to have hypovolemia or pericardial tamponade require volume expansion and vasopressors to maintain end-organ perfusion.28 If there is evidence of coronary artery occlusion and myocardial dysfunction, inotropic therapy may be required. Preoperative imaging may demonstrate occlusion of aortic branch vessels, which can cause progressive acidosis and shock due to organ malperfusion. In these patients, hemodynamic support should be provided until flow can be reestablished to the occluded vessel via surgical repair.
Induction and Monitoring
Intraoperative management of the patient presenting for repair of a TAAD should focus on maintaining hemodynamic stability and avoiding acute increases in blood pressure, which may precipitate aortic rupture.29 Arterial pressure monitoring should proceed with consideration of the pathophysiology of the aortic dissection and the surgical plan in mind, and invasive arterial pressure monitoring combined with intraoperative neuromonitoring may be used to improve sensitivity for malperfusion. If antegrade cerebral perfusion (ACP) with hypothermic circulatory arrest is planned, arterial pressure monitoring in both the right upper extremity and either left upper extremity or femoral artery is necessary to allow for pressure monitoring during ACP and systemic CPB, respectively.30 The right radial artery may provide falsely elevated readings during CPB if right axillary or innominate cannulation is used. If retrograde cerebral perfusion (RCP) is planned, placement of an internal jugular or subclavian central venous catheter is necessary to allow for pressure monitoring during RCP.
The high risk of neurological dysfunction after TAAD repair requires a higher level of intraoperative neuromonitoring. Cerebral monitoring can be accomplished using jugular venous oxygen saturation monitoring, electroencephalography (EEG), or near-infrared spectroscopy (NIRS).31 Jugular venous oxygen saturation is a measure of global cerebral oxygen supply and demand, but it requires additional invasive catheter placement and has not been reliably shown to predict outcome after aortic surgery.32
EEG is sometimes used to evaluate for electrocerebral silence before the initiation of hypothermic circulatory arrest. EEG can also detect abnormal recovery or seizure activity after circulatory arrest and during rewarming, which can be associated with adverse neurological outcomes.33–35 The use of full EEG monitoring during a TAAD repair is uncommon, owing to the complexity of monitor application in the setting of an emergent surgical procedure and the need for additional training to reliably interpret EEG. More frequently, processed EEG monitors such as the bispectral index (BIS) are used to assess depth of anesthesia and the presence of electrocerebral silence in patients undergoing TAAD repair. Although the BIS value appears to decrease reliably with progressive hypothermia, it only monitors the frontal cortex and is vulnerable to a number of artifacts common in patients undergoing cardiac surgery.36–38 These artifacts include high-dose opioids, the use of N-methyl-D-aspartate (NMDA) receptor antagonists, neuromuscular blocking agents, and even forced-air warming devices.38 The value of BIS or EEG-guided electrocerebral silence in improving neurocognitive outcome remains unclear.
NIRS allows for the noninvasive evaluation of regional cerebral oxygen saturation and is commonly used for neuromonitoring in aortic surgery.39,40 The average baseline value is between 60% and 70% and should be measured on room air in the absence of sedatives or opioids, if possible.31,41 Although NIRS typically allows for reliable monitoring of cerebral oxygen saturation, it does have a number of limitations. NIRS monitoring is limited to the frontal cortex, and measurements may be affected by extracerebral tissues and changes in the ratio of cerebral venous to arterial blood volume. It can also be affected by patient-specific derangements, including hemodilution, elevated bilirubin, and pathological alterations in cerebral autoregulation.40,42 Previous studies have shown broad variation in the threshold values for absolute and relative cerebral desaturation, which are associated with postoperative neurocognitive deficits, but it appears that both the degree and duration of desaturation are important in predicting adverse outcomes.42,43 In aortic surgery, a decrease in the regional cerebral oxygen saturation to ≤55% or 76%–86% of baseline has been associated with an increase in postoperative neurological events.44,45 Importantly, the use of NIRS may allow for early identification of technical issues, such as cannula malposition, that may cause catastrophic neurological injury if left uncorrected.46
The management of regional cerebral oxygen desaturation and its ability to improve neurological outcome continue to evolve. Denault et al47 have proposed a treatment algorithm for cerebral desaturation that includes optimization of cannula and head position, augmentation of mean arterial pressure and oxygen saturation, avoiding hypocarbia, and increasing systemic oxygen delivery through transfusion and increasing cardiac output (Table 2).31 The effect of this algorithm on neurological outcome remains under investigation.48 A recent meta-analysis examining the use of NIRS in patients undergoing cardiac surgery showed no significant difference in mortality, stroke, red blood cell transfusion, or resource utilization.49 Two large studies examining postoperative cognitive dysfunction showed differing results, with 1 demonstrating the utility of NIRS in predicting cognitive decline after cardiac surgery and another showing no benefit.50,51 Similarly, a recent randomized controlled trial showed that correction of cerebral oxygen desaturation during cardiac surgery was not associated with a decrease in postoperative delirium.52 Of note, there is currently minimal literature examining the utility of NIRS exclusively in aortic surgery with hypothermic circulatory arrest. Overall, there is weak evidence that the active management of cerebral oxygen desaturation is associated with improved neurocognitive outcome, but the potential of NIRS to identify modifiable technical issues compromising cerebral perfusion justifies its routine use in TAAD repair.
TEE is critical to the management of patients presenting to the operating room with TAAD. After the induction of anesthesia, TEE examination should be undertaken to confirm the presence of the aortic dissection before proceeding with central venous access and surgery (Figure 1).53 The echocardiographer should be aware of possible TEE artifacts that may be confused for a dissection. A true TAAD is characterized by random dissection flap movement, consistent echo intensity, and a clear change in color-flow Doppler signal around the dissection flap. In contrast, reverberation and side lobe artifacts are typically static and do not cause changes in the color-flow Doppler signal.54 Patients with ascending aortic dilation may also demonstrate mirror artifacts from the left atrium or right pulmonary artery that may be mistaken for a TAAD.55
Similar to preoperative TTE, TEE evaluation in a patient with TAAD should focus on assessing for complications that may alter surgical management. The presence of left ventricular regional wall motion abnormalities suggests coronary ostia obstruction or dissection and may indicate the need for revascularization. Proximal extension of the dissection into the aortic annulus may also result in acute AI, and rupture of the dissection into the pericardium may cause pericardial tamponade.21,56 Similarly, TEE may be used to assess for pleural effusion, which can suggest leaking of blood from the dissected aorta.
Measurement of the dimensions of the aortic annulus, sinuses of Valsalva, and the sinotubular junction can help guide whether surgical repair includes the ascending aorta alone or also includes the aortic root and/or the aortic valve. If present, the mechanism and severity of AI should be defined to help guide whether surgical repair includes aortic valve repair or replacement. Multiple mechanisms may be responsible for AI in TAAD, including (1) annular dilation from a preexisting thoracic aortic aneurysm, (2) aortic valve leaflet disruption from proximal extension of the dissection into the aortic root, (3) prolapse of the dissection flap through an anatomically normal aortic valve, or (4) preexisting aortic valve pathology.57 If the aortic valve is anatomically normal, valve resuspension can often be performed.21 Aortic valve pathology is typically assessed using the midesophageal long-axis and midesophageal aortic valve short-axis views with and without color-flow Doppler, although other modalities, including 3-dimensional TEE, may provide additional information in select cases.58,59
TEE can also be used to assess the extent of the entry tear. Unfortunately, the location of the aortic arch in relation to the trachea can make it difficult to obtain satisfactory images of the arch vessels, and assessment of the branches of the descending thoracic aorta is typically nondiagnostic.56 Vegas and Jerath60 have previously described the approach to and limitations of imaging the ascending aorta and aortic arch. The use of a fluid-filled balloon in the trachea to allow for visualization of the aortic arch by TEE has been described, but this procedure is not commonly performed.61 If preoperative CT or magnetic resonance imaging is inconclusive or evolution of the dissection is suspected, epiaortic imaging of the aortic arch can be performed.62,63
Differentiation of the true from the false lumen should be made echocardiographically (Figure 2). The true lumen is characterized by systolic expansion, whereas the false lumen typically expands in diastole.56 The false lumen may also demonstrate either spontaneous echocardiographic contrast or hematoma, further assisting in differentiation.56 Identification of the true lumen is important to assist in guiding aortic cannulation via the Seldinger technique, via either retrograde or anterograde passage of a wire into the true lumen with subsequent placement of the arterial cannula.64 If elevated line pressure is noted on the initiation of CPB, immediate reevaluation should be performed to ensure that the previously identified true lumen is receiving blood flow from the CPB circuit because pressurization of the false lumen with the initiation of CPB may result in rapid propagation of the dissection and aortic rupture.
After surgical repair, the aorta should be reexamined to ensure that the entry tear and false lumen have been excluded and that flow has been restored to the true lumen.21 The aortic valve should be interrogated to confirm that no significant AI persists after repair or replacement.21 New left ventricular regional wall motion abnormalities may indicate the need for further coronary intervention, either via coronary artery bypass grafting or percutaneous coronary intervention. Global assessment of right and left ventricular function is important to evaluate for the need for more aggressive inotropic support to prevent postoperative low cardiac output syndrome, which is associated with an increase in mortality after TAAD repair.65
Pericardial Tamponade in Aortic Dissection
Pericardial tamponade is a potentially fatal complication of aortic dissection. Although immediate femoral venous and arterial cannulation can be used to allow for the early initiation of CPB if resuscitative efforts are failing, surgical or percutaneous drainage is preferable if possible.66,67 The approach to patients with a TAAD with tamponade depends on a number of factors, including the degree of hemodynamic instability, whether they are able to cooperate for percutaneous needle pericardiocentesis, and whether other factors make them candidates for inhalational induction of anesthesia with maintenance of spontaneous ventilation (ie, nil per os status, suspected mesenteric ischemia), which is ideal in patients with tamponade. Patients with cardiogenic shock should be prepped and draped for immediate surgical drainage after the induction of anesthesia in the event of hemodynamic collapse.68 Of note, pulsus paradoxus may not be present in patients with a TAAD because of the frequent occurrence of severe AI.
Decompression of a pericardial effusion in a patient with a TAAD requires special care because sudden decompression of the pericardial sac may result in uncontrolled hypertension and potentially aortic rupture. Controlled drainage of the effusion combined with gradual downward titration of vasopressors and inotropes should occur, and either arterial or venous dilators may be used temporarily to control blood pressure.66
Surgical Aortic Reconstruction
The type of surgical repair depends on a number of important principles: (1) involvement of the aortic root, (2) status of the aortic valve and associated AI, and (3) involvement of the aortic arch. The main objective of surgical repair is the resection of the dissection tear in the ascending aorta or arch, obliterating the false lumen and redirecting flow into the true lumen.69 Patients undergoing surgical repair must have a thorough evaluation of the aortic valve via TEE and by visual inspection once the aorta is opened. If there is AI, but the aortic valve appears morphologically normal, the valve can often be “resuspended,” reanchoring the aortic valve commissures to establish coaptation of the leaflets.70 There are a number of scenarios where more aggressive repair of the aortic valve/root is warranted. These scenarios include (1) patients with connective tissue disease, (2) dissection or damage of the sinus of Valsalva, (3) the presence of annuloaortic ectasia or primary aortic valve disease, and (4) root dissection or aneurysm meeting repair criteria.71
Given these considerations, the specific surgical repair will depend on the pathology present. If the involvement is limited to the noncoronary sinus, a uni-Yacoub procedure is used to replace only that sinus and the ascending aorta.72 If there is aortic root involvement, it may be replaced with or without the replacement of the aortic valve. If both are replaced, this can be done using a composite valve graft (Bentall procedure; Figure 3A) or, in some circumstances, a valve-sparing root replacement (David procedure; Figure 3B).73,74 Valve-sparing operations in patients with bicuspid aortic valves undergoing aortic root reconstruction remain controversial, although recent series have demonstrated acceptable clinical outcomes in this patient population.75,76 Procedures involving the aortic root require the reimplantation of the coronary arteries, which may add to operative risk (Figure 3). The extent of arch replacement in the setting of TAAD remains controversial and varies by institution, with data suggesting that reintervention is more a function of long-term follow-up and management than the extent of aortic arch replacement.77
The optimal surgical approach to management of TAAD is determined by multiple factors, including underlying patient pathology, aortic valvular involvement, and institutional preference.71,78 An understanding of the potential surgical options, rationales for each, and the approaches to cerebral perfusion is useful to allow for active monitoring during CPB, as well as to tailor the echocardiographic assessment of the aorta after surgical repair.
Cerebral Perfusion and Monitoring
Surgery involving the aortic arch frequently requires interruption of systemic circulation with or without selective perfusion of the cerebral vasculature. With the advent of ACP and RCP, there has been a shift in aortic surgery from deep hypothermic circulatory arrest (14°C–20°C) to more modest degrees of systemic cooling, with equivalent or improved neurological outcomes.53,79–83
Selective cerebral perfusion is commonly used in aortic cases requiring hypothermic circulatory arrest to maintain cerebral blood flow and attempt to minimize neurological injury. The 2 most common strategies include ACP and RCP. In ACP, blood is directed from the axillary or innominate artery in an antegrade direction up the right common carotid artery to provide perfusion to the brain after clamping of the innominate artery and discontinuation of systemic blood flow (Figure 4).78 While ACP is advantageous because it maintains continuous circulation through the arterial system, it can result in embolization or vascular injury during manipulation of the arch vessels and risks nonuniform perfusion of the brain if only unilateral ACP is used.84,85
Monitoring of perfusion pressure during ACP can be accomplished via arterial blood pressure monitoring in the right upper extremity. ACP is typically performed by targeting cerebral blood flow, with values near 10 mL/kg/min used most frequently.86,87 Current evidence suggests that flow >6 mL/kg/min is necessary to meet cerebral metabolic requirements.88 The optimal perfusion pressure for ACP is unclear, with equivalent neurological outcomes demonstrated in patients managed with high (≈80 mm Hg) versus low (≈50 mm Hg) pressures.89 There is limited animal evidence that high cerebral perfusion pressures (90 mm Hg) may be associated with an increase in intracranial pressure and worse neurocognitive outcome.90 If NIRS is used for intraoperative neuromonitoring, it can help detect cannula malposition, if present, and guide the decision to use bilateral ACP.91–93 A small patient series used a decrease in the left regional cerebral oxygen saturation to <55% and/or a decrease of 15%–20% below baseline as a threshold to initiate bilateral ACP. This process was associated with a significant increase in left-sided cerebral oxygen saturation after initiation of bilateral ACP and no postoperative neurological deficits.92
In RCP, blood is directed in a retrograde direction through the internal jugular veins and cerebral venous sinuses to provide flow of oxygenated blood through the brain during circulatory arrest.78 This technique consistently provides bilateral perfusion through the cerebral venous sinuses and can promote flushing of embolic material from the cerebral vasculature, but its use is limited by concerns about cerebral edema and inadequate neuroprotection due to decreased overall cerebral blood flow.84,85 Technically, RCP is typically accomplished utilizing a bicaval cannulation technique. When RCP is initiated, the superior vena cava cannula is snared, the arterial cannula is clamped, and oxygenated blood is given retrograde through the superior vena cava into the cerebral venous system.94 RCP pressure can be assessed using the central venous pressure reading from an internal jugular or subclavian central venous catheter and typically ranges from 15 to 25 mm Hg, with a maximum pressure of approximately 40 mm Hg.94
While ACP remains the most common method of cerebral perfusion during aortic surgery, the clinical benefit of ACP over RCP remains a topic of continued debate.95–98 The use of combined ACP and RCP during circulatory arrest has been proposed, but this approach has yet to be rigorously evaluated.99
Neuroprotective Strategies During Hypothermic Circulatory Arrest
Numerous drugs have been used to attempt to provide protection to the brain and spinal cord during aortic surgery, and broad institutional variation exists regarding which specific drugs are used for neuroprotection.11,100,101 Steroids, barbiturates, propofol, and mannitol are most commonly used for neuroprotection in aortic surgery.11,101 In a recent, large, retrospective analysis of patients with a TAAD, corticosteroid use was associated with a decreased risk of new permanent postoperative neurological dysfunction, although the specific dose, timing of administration, and corticosteroid type were not defined.11 Mannitol and barbiturates were not found to be neuroprotective.11 Propofol may also be used to decrease cerebral metabolic oxygen consumption and induce burst suppression on EEG.100 However, no studies to date have focused specifically on propofol in hypothermic circulatory arrest, and propofol-induced burst suppression has not been shown to improve neurological outcomes in previous studies of patients undergoing cardiac surgery.102
The use of topical cerebral cooling during circulatory arrest is controversial, and evidence is limited for its efficacy. Most evidence is limited to animal studies of deep hypothermic circulatory arrest, with data suggesting better cerebral cooling and neurobehavioral outcomes in animals who had topical ice application.103 Human evidence in deep hypothermic circulatory arrest is limited, with 1 study of pulmonary thromboendarterectomy patients showing a tympanic membrane temperature consistently lower than the bladder or rectal temperature when topical cooling was used.104 Although topical cooling is a low-risk intervention, it may also interfere with other monitors of cerebral perfusion and has the potential to cause ocular or tissue injury. With the frequent utilization of selective cerebral perfusion, there is likely minimal benefit to the routine use of topical cooling in TAAD surgery.
Patients with a TAAD may present with symptoms of ischemia related to malperfusion of the abdominal viscera, kidneys, or lower limbs, which is associated with a significant increase in mortality after TAAD repair.105,106 This outcome can be a result of either dissection into the origin of a vessel or from compression of the true lumen by the dissection flap.107 These patients may benefit from surgical fenestration of the intimal flap to reverse ischemia. In surgical fenestration, an opening is created between the true and false lumens, frequently with insertion of a vascular stent to maintain patency of the connection between the 2 lumens.106,108 This technique has been used successfully in patients with both TAAD and type B aortic dissection, with relief of ischemic symptoms in nearly 90% of patients.106,108
Alternatively, some patients with malperfusion may be managed with endovascular stent graft placement to restore flow to ischemic viscera. This procedure can be performed alone or in combination with aortic fenestration.109 Patients with genetic aortopathy or entry tears originating in the aortic arch may benefit from more extensive combined aortic arch procedures with extension into the descending thoracic aorta, such as a conventional or frozen elephant trunk placement to facilitate thoracic endovascular aortic repair (TEVAR). TEVAR can be performed at the time of the initial operation in patients with malperfusion or delayed to allow for staged repair.110 Although TEVAR may be beneficial in alleviating malperfusion, it does increase the risk of spinal cord ischemia. In patients with significant malperfusion, some authors have advocated delaying ascending aortic repair to allow for resolution of visceral ischemia, although the risks of delaying surgery in patient with a TAAD must be considered.111
With current endovascular technology, it is estimated that 30%–40% of patients with a TAAD are potentially candidates for endovascular repair.112,113 For ascending aortic stent graft placement, a number of criteria must be met. The entry tear must originate distal to the sinotubular junction, with an adequate proximal landing area. There also must be an adequate distal landing area proximal to the takeoff of the innominate artery. Significant AI requiring surgical repair, coronary artery dissection, or cardiac tamponade generally excludes the endovascular approach. Patients with a history of coronary artery bypass grafting with grafts originating from the ascending aorta also cannot undergo endovascular TAAD repair.112–114 This procedure is most frequently performed via a transfemoral approach, although the transapical and transcarotid approaches have also been described.115,116 Outcome data are currently limited primarily to case series, but endovascular TAAD repair has shown acceptable results in high-risk surgical candidates.116
MANAGEMENT OF COAGULOPATHY AFTER CPB
Perioperative bleeding and the need for blood product transfusion are common in aortic surgery.117 The pathophysiology of bleeding in TAAD is complex, but recent literature suggests that the dissection activates the hemostatic system, leading to intense fibrinolysis, platelet activation, and clotting factor consumption.118,119 Tissue factor exposure in the false lumen causes excess thrombin generation that is amplified by exposure to CPB.120 Studies using thromboelastography to characterize the nature of coagulopathy in TAAD suggest that this preexisting coagulopathy coupled with surgery and hypothermia leads to a progressive reduction in clotting factors, platelet function, and fibrinolysis, resulting in a coagulopathic derangement similar to disseminated intravascular coagulation.118
Despite this recent evidence, little clinical data exist to drive decision making in patients with significant surgical bleeding after TAAD repair. The optimal approach to the management of coagulopathy after aortic surgery consists of (1) use of point-of-care laboratory studies (eg, thromboelastometry) to drive decision-making; (2) aggressive goal-directed replacement of fibrinogen, platelet, and factor deficiencies; (3) use of antifibrinolytic agents to decrease blood component requirements; and (4) consideration for the use of factor concentrates to help prevent transfusion-related complications.121–129
The use of rotational thromboelastometry (ROTEM; Tem International GmbH, Basel, Switzerland) to direct blood component replacement is likely beneficial in patients undergoing aortic surgery. The use of thromboelastometry to provide decision support for replacement of factor and fibrinogen deficiency in both thoracoabdominal aortic aneurysm repair and ascending aortic surgery has been shown to decrease intraoperative transfusion requirements as compared to either empiric transfusion or transfusion strategies based on standard laboratory tests.124,125,130 Furthermore, thromboelastometry-guided protocols in acute aortic dissection have been shown to reduce rates of surgical reexploration, massive transfusion, and the cost of transfusion.130,131
In addition to factor and fibrinogen depletion, platelet dysfunction is common after TAAD repair, and functional assays of platelet function are useful to help determine the need for additional platelet transfusion.128,132 The platelet response to TAAD is complex, with initial activation resulting in decreased overall platelet function and a concomitant decrease in platelet count.118,119,133 Moreover, the anatomical extent of the dissection correlates with platelet activation and inflammation.134 Given the variability seen in platelet function and platelet count after TAAD repair, decisions regarding the need for additional platelet transfusion should be made with attention to both platelet counts and thromboelastometry results.128
Antifibrinolytic agents in cardiac surgery have been shown to decrease perioperative transfusion requirements and are recommended for routine use in current guidelines.135–137 The most commonly used antifibrinolytic agents in cardiac surgery are the lysine analogues ε-aminocaproic acid (EACA) and tranexamic acid (TXA).138 Although some retrospective data indicate that TXA is more effective in reducing blood loss compared to EACA, a recent prospective trial in patients undergoing thoracic aortic surgery found no difference in cumulative blood loss, total packed red blood cells, and total blood product requirements.123,139 However, EACA was associated with a higher incidence of postoperative renal failure, while patients receiving TXA had a higher incidence of postoperative seizure.139 This finding was consistent with a larger retrospective review that examined TXA and EACA in patients undergoing cardiac surgery.140
The off-label use of plasma-derived complex concentrates for the correction of coagulopathy after cardiac surgery has been an area of intense recent investigation.141–144 Prothrombin complex concentrates (PCCs) have been used for the reversal of warfarin in patients undergoing cardiac surgery, and recent evidence suggests that the use of PCCs to correct postoperative coagulopathy after cardiac surgery is associated with a decrease in postoperative bleeding, massive transfusion, and surgical reexploration.141,143,144 A recent, large, retrospective study showed that first-line therapy with coagulation factor concentrates combined with point-of-care testing decreased transfusion requirements and thrombotic complications, with near elimination of the need for fresh frozen plasma transfusion, although this protocol was also associated with an increase in platelet and fibrinogen concentrate utilization.143 One observational study in patients undergoing cardiac surgery showed an increase in acute kidney injury after PCC administration, but this finding has not been consistently identified in other studies.141,144 In patients with a TAAD with refractory bleeding, recombinant activated factor VII has been successfully used as salvage therapy, although concerns about thrombotic complications persist with its utilization.145–147
An understanding of how the activation of the hemostatic system in patients with a TAAD contributes to the pathophysiology of coagulopathy is essential for appropriate management. A goal-directed approach with an emphasis on fibrinogen, factor replacement, and antifibrinolytic therapy appears to decrease overall transfusion requirements and may improve outcomes.
The care of patients undergoing TAAD repair requires a concerted effort on the part of the anesthetic and surgical teams. Early diagnosis and aggressive preoperative management are critical to expediting surgical repair. An appropriately tailored management plan with therapeutic interventions guided by underlying patient pathology, thoughtful TEE imaging, advanced monitoring, and laboratory evaluation can be used to improve care and outcomes for this patient population.
The authors thank Lauren Halligan, MSMI (Department of Surgery, Duke University Medical Center, Durham, NC), for illustrations of Figures 3 and 4.
Name: Stephen H. Gregory, MD.
Contribution: This author helped with conceptualization, original draft preparation, and manuscript review and editing.
Name: Suraj M. Yalamuri, MD.
Contribution: This author helped with conceptualization, original draft preparation, and manuscript review and editing.
Name: Muath Bishawi, MD.
Contribution: This author helped prepare the original draft, and review and edit the manuscript.
Name: Madhav Swaminathan, MD, MMCi, FASE, FAHA.
Contribution: This author helped with conceptualization, original draft preparation, and manuscript review and editing.
This manuscript was handled by: Roman M. Sniecinski, MD.
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