Anesthesia for open abdominal aortic surgery

INTRODUCTION — 

Open aortic surgery is used for patients who have indications for abdominal aortic aneurysm (AAA) repair but unfavorable anatomy for endovascular aortic repair, for those undergoing endovascular repair and require conversion from an endovascular to open surgical approach, as well for those with infected aortic grafts requiring explantation. Similarly, while endovascular techniques are often successful in managing aortoiliac occlusive disease or acute aortic thrombosis, an open surgical approach may become necessary when these are unsuccessful at restoring perfusion. Open aortic surgery is also required to manage aortic rupture from any cause (eg, ruptured AAA, ruptured aortic dissection, traumatic rupture). The principles discussed below also apply to other types of surgery requiring control of the abdominal aorta, such as for open surgical management of isolated iliac artery aneurysms (external iliac, internal iliac) and visceral artery aneurysms.

This topic will review anesthetic management for patients undergoing open abdominal aortic surgery. Anesthetic management for other types of vascular surgery is discussed in separate topics:

●(See "Anesthesia for aortic surgery with hypothermia and elective circulatory arrest in adult patients".)

●(See "Anesthesia for open descending thoracic aortic surgery".)

●(See "Anesthesia for carotid endarterectomy and carotid stenting".)

●(See "Anesthesia for endovascular aortic repair".)

●(See "Anesthesia for infrainguinal revascularization".)

PREANESTHETIC CONSULTATION — 

The preanesthetic consultation for elective open abdominal aortic surgery focuses on assessing perioperative risks and consulting with the surgeon and other specialists to minimize risks.

Considerations for emergency procedures are discussed below. (See 'Emergency aortic surgery' below.)

Risk assessment

●Cardiovascular risk – Patients with aortic vascular disease typically have other manifestations of cardiovascular disease and are at high risk for cardiovascular complications (table 1 and table 2) [1,2]. In nearly 23,000 patients having open aortic surgery included in the National Surgical Quality Improvement Program (NSQIP) database in the years between 2005 and 2013, postoperative myocardial infarction occurred in 3.0 percent, cardiac arrest in 3.2 percent, and mortality in 8.7 percent [3].

We obtain a preoperative electrocardiogram (ECG), which is useful as a baseline for comparison with any postoperative ECGs. Risk assessment to determine whether additional cardiac testing (eg, stress testing or echocardiography) is warranted is discussed separately. (See "Evaluation of cardiac risk prior to noncardiac surgery", section on 'Testing to further define risk'.)

●Pulmonary risk – Many patients undergoing abdominal aortic surgery are current or former tobacco users with chronic obstructive pulmonary disease (COPD). Smoking cessation is recommended before elective aortic surgery. Evaluation and management of these and other pulmonary risks are discussed in separate topics:

•(See "Anesthesia for patients with chronic obstructive pulmonary disease", section on 'Preanesthesia consultation'.)

•(See "Smoking or vaping: Perioperative management".)

•(See "Evaluation of perioperative pulmonary risk".)

•(See "Strategies to reduce postoperative pulmonary complications in adults", section on 'Preoperative strategies'.)

●Renal risk – Open aortic repair carries a high risk for perioperative acute tubular necrosis (ATN) and acute kidney injury (AKI) [4]. Elevated preoperative serum creatinine is the strongest predictor of postoperative kidney dysfunction after open aortic surgery and is also a predictor of cardiovascular complications and mortality (table 1) [5-7]. Other preoperative risk factors include exposure to intravenous contrast or other nephrotoxins, anemia, and the need for emergency surgery, particularly for ruptured abdominal aortic aneurysm (AAA) [4,8]. Intraoperative factors that exacerbate kidney ischemia include suprarenal or juxtarenal aortic cross-clamping, prolonged cross-clamping, embolism of atherosclerotic debris into the renal arteries, and prolonged hypotension. (See "Procedure-specific and late complications of open aortic surgery in adults", section on 'Acute kidney injury'.)

Perioperative techniques to minimize the incidence of ATN and AKI include [4,8,9]:

•Avoidance of preoperative, intraoperative, and postoperative anemia – (See 'Fluid and transfusion management' below and "Perioperative blood management: Strategies to minimize transfusions", section on 'Treatment of anemia and iron deficiency' and "Possible prevention and therapy of ischemic acute tubular necrosis".)

•Planned use of cell salvage techniques to minimize transfusions – (See 'Blood salvage and transfusion' below and "Surgical blood conservation: Intraoperative blood salvage".)

•Adequate preoperative hydration and intraoperative maintenance of intravascular volume – (See 'Hemodynamic management' below and "Intraoperative fluid management", section on 'Hypovolemia' and "Intraoperative fluid management", section on 'Monitoring intravascular volume status'.)

Preoperative laboratory testing — We examine preoperative laboratory tests that routinely include complete blood count, tests of hemostasis, electrolytes, glucose, blood urea nitrogen [BUN], creatinine to provide baseline values for comparison with intraoperative point-of-care and postoperative tests.

Typing and crossmatching are performed for up to two units of packed red blood cells (RBCs) to be available in the operating room before surgical incision (see "Open surgical repair of abdominal aortic aneurysm", section on 'Blood for transfusion'). The presence of unusual antibodies requires preoperative planning in consultation with institution-specific (blood bank) resources [10]. (See 'Blood salvage and transfusion' below and "Surgical blood conservation: Intraoperative blood salvage".)

Management of medications — Perioperative cardiovascular, thrombotic, and infectious complications are minimized by continuing chronic medications and managing the administration of prophylactic medications:

●Cardiovascular medications – Statins, beta blockers, and aspirin are continued in patients receiving these therapies (see "Management of cardiac risk for noncardiac surgery"). Preoperative management of other cardiovascular medications is reviewed elsewhere. (See "Perioperative medication management", section on 'Cardiovascular medications'.)

●Anticoagulant and antiplatelet medications – Chronically administered anticoagulant or antiplatelet medications are timed to allow safe placement of an epidural catheter as feasible (table 3). (See "Neuraxial anesthesia/analgesia techniques in the patient receiving anticoagulant or antiplatelet medication".)

Planning for postoperative pain management — Because of the abdominal incision required to access the aorta, patients undergoing open aortic surgery have significant postoperative pain, which contributes to morbidity [11,12]. Continuous thoracic epidural analgesia (TEA) is typically used to provide superior postoperative pain management with minimal respiratory depression (see 'Postoperative pain management' below), and may reduce the risk of myocardial infarction, respiratory failure, and arterial graft occlusion, as well as facilitate early recovery of bowel function [12-19]. The techniques, risks, and benefits of epidural catheter placement are discussed with the patient, and an examination of the back is performed during the preanesthesia consultation.

INTRAOPERATIVE MANAGEMENT

Monitoring

Intravascular monitors

●Peripheral venous access – Two large bore peripheral intravenous catheters are often inserted with one attached to a fluid warmer. If a sheath introducer (eg, Cordis) is used, one large bore peripheral IV may provide adequate additional vascular access.

●Intra-arterial catheter – An intra-arterial catheter is always inserted, ideally before anesthetic induction. It is used for:

•Continuous monitoring of arterial blood pressure (BP) for early detection of intraoperative hypotension. However, mean arterial BP is a poor surrogate of cardiac index and if there is concern for myocardial ischemia or dysfunction, additional monitoring will be necessary [20]. (See "Anesthesia for noncardiac surgery in patients with ischemic heart disease", section on 'Monitoring for myocardial ischemia'.)

•Evaluation of respirophasic variations in the arterial pressure waveform to assess fluid responsiveness (figure 1). (See "Intraoperative fluid management", section on 'Dynamic parameters to assess volume responsiveness'.)

•Intermittent blood sampling for point-of-care (POC) testing – We obtain several sets of measurements during open aortic surgery: baseline values (after induction), after the aortic cross-clamp (AXC) has been placed and just before its removal, and again before emergence and extubation (see 'Management of aortic unclamping' below). POC testing typically includes arterial blood gases, pH, hemoglobin, electrolytes, glucose, and activated clotting time (ACT). Available tests of hemostasis are employed when there is evidence of coagulopathy or significant bleeding [21]. (See "Intraoperative transfusion and administration of clotting factors", section on 'Point-of-care tests' and "Point-of-care hemostasis testing (viscoelastic tests)".)

Patients with abdominal aortic aneurysm (AAA) often have peripheral arterial atherosclerosis and may have discrepancies in BP between the right and left upper extremities. Generally, the brachial artery, associated with an increased risk of complications, is avoided. Routine use of ultrasound guidance facilitates catheterization of the radial artery. (See "Intra-arterial catheterization for invasive monitoring: Indications, insertion techniques, and interpretation", section on 'Site selection' and "Intra-arterial catheterization for invasive monitoring: Indications, insertion techniques, and interpretation", section on 'Use of ultrasound guidance'.)

●Central venous access – A sheath introducer (eg, Cordis) for central venous access can provide large-bore venous access for fluid and blood administration and vasoactive drug infusions or introduction of a central venous catheter. The need for a pulmonary artery catheter (PAC; ie, Swan-Ganz catheter) is rare but may be helpful in treating severe right ventricular (RV) dysfunction or severe pulmonary hypertension. In patients with central venous access, central venous pressure (CVP) is typically measured and provides supplemental data; however, it is a poor predictor of intravascular volume status and fluid responsiveness. (See "Intraoperative fluid management", section on 'Traditional static parameters'.)

Transesophageal echocardiography — We typically insert a transesophageal echocardiography (TEE) probe to monitor cardiac function and intravascular volume status during open abdominal aortic surgery because of the high risk for severe hemodynamic instability and adverse perioperative cardiovascular events, particularly during aortic cross-clamping and unclamping. (See 'Hemodynamic management' below.)

During these cases, TEE monitoring is used to:

●Avoid hypovolemia or hypervolemia.

●Detect regional and global ventricular dysfunction. New regional wall motion abnormalities (RWMAs) (eg, hypokinesis or akinesis) have a higher sensitivity for detecting ischemia than either electrocardiogram (ECG) or PAC changes (figure 2 and figure 3). Although no data are available to demonstrate that TEE monitoring can decrease the incidence of adverse cardiovascular outcomes, early recognition of myocardial ischemia or ventricular dysfunction facilitates management. (See "Anesthesia for noncardiac surgery in patients with ischemic heart disease".)

Aortic cross-clamping can cause a sudden, large increase in left ventricular (LV) systolic afterload, leading to myocardial ischemia or LV failure with hemodynamic instability [22-28]. RWMAs may progressively worsen after placement of the AXC, with progression to severe global hypokinesis. TEE indicators of poor global LV systolic or diastolic function predict postoperative cardiopulmonary failure and prolonged intubation after abdominal aortic surgery [29,30]. (See 'Management of aortic cross-clamping' below.)

●Assess causes of hypotension. Examples include decreased preload due to venodilation or myocardial dysfunction due to acidosis after aortic unclamping. (See 'Management of aortic unclamping' below.)

●Detect aortic pathology, such as atheromas or aortic dissection resulting from cannulation or cross-clamping of the aorta.

●Detect thromboembolism or air embolism.

The use of intraoperative TEE monitoring is discussed in more detail separately. (See "Intraoperative transesophageal echocardiography for noncardiac surgery".)

Even if TEE is not used electively, rapid deployment may be urgently needed to diagnose causes of unanticipated cardiovascular collapse (ie, "rescue" TEE). (See "Intraoperative rescue transesophageal echocardiography (TEE)".)

Other monitors — Standard noninvasive monitoring includes continuous ECG monitoring with leads II and V₅ and with computerized ST-segment trending to detect myocardial ischemia or arrhythmias. (See "Anesthesia for noncardiac surgery in patients with ischemic heart disease", section on 'Monitoring for myocardial ischemia'.)

A bladder catheter is inserted after induction to measure urine output. The temperature probe in this catheter or the oropharyngeal temperature is continuously monitored to avoid hypothermia. (See 'Temperature management' below.)

Similar to open descending thoracic aortic surgical procedures, cerebral oximetry is often used (see "Anesthesia for open descending thoracic aortic surgery", section on 'Cerebral oximetry to monitor for cerebral ischemia'). Processed electroencephalographic monitoring (eg, bispectral index [BIS]) may also be used [31].

Anesthetic management — Open abdominal aortic surgery uses either a midline incision (typically from the xiphoid to the pubis), a retroperitoneal abdominal incision, or a thoracoabdominal incision. These large incisions are painful postoperatively and associated with an increased risk for pulmonary and other complications. (See "Open surgical repair of abdominal aortic aneurysm", section on 'Incision and aortic exposure' and "Overview of damage control surgery and resuscitation in patients sustaining severe injury", section on 'Midline incision'.)

As such, we typically use an intraoperative anesthetic technique that combines general anesthesia (GA) and thoracic epidural anesthesia (TEA). The addition of epidural anesthesia during GA attenuates responses to painful stimuli intraoperatively, thereby allowing reductions in intraoperative anesthetic and opioid dosing and possibly facilitating early extubation in or shortly after leaving the operating room [32,33]. Postoperatively, TEA provides continuous pain control, improving patient mobilization and reducing pulmonary complications, as discussed below. (See 'Postoperative pain management' below.)

Epidural anesthesia

Catheter placement — We place the catheter in the immediate preoperative period or in the operating room shortly before induction of general anesthesia (GA), at least one hour before the planned intraoperative administration of a bolus of intravenous unfractionated heparin. (See "Neuraxial anesthesia/analgesia techniques in the patient receiving anticoagulant or antiplatelet medication", section on 'Intravenous UFH'.)

We use the T8 to T10 level for planned transperitoneal incision or the T9 to T11 level for planned retroperitoneal incision. Although some authors recommend a higher T6 to T7 level to achieve optimal postoperative pain control [14,34,35], most have suggested the T9 to T12 level to attain the advantages of TEA while minimizing hemodynamic instability [13,36-38]. Also, higher levels may not provide adequate analgesia for patients with more distal surgery (eg, iliofemoral dissection), and further cephalic spread does not offer additional benefits. A lumbar epidural technique is a reasonable alternative if thoracic catheter placement is technically challenging due to anatomic considerations. This option may be as effective for postoperative analgesia, particularly if an opioid is added to the continuous epidural infusion [39-41]. Immediately after inserting the epidural catheter, a test dose is administered to exclude possible intravascular or intrathecal spread and ensure that the block will be effective for intraoperative use. If the epidural is found to be inadequate following insertion and testing, the catheter may need to be replaced at a different level since a functional epidural is required for post-operative pain management. Details regarding techniques for epidural catheter placement and test dose administration are described separately. (See "Epidural and combined spinal-epidural anesthesia: Techniques", section on 'Epidural anesthesia technique' and "Epidural and combined spinal-epidural anesthesia: Techniques", section on 'Epidural test dose'.)

Intraoperative dosing — In a hemodynamically stable patient, an initial bolus of local anesthetic is typically administered before the surgical incision to establish the block. The bolus is administered in 2 mL increments (up to 10 mL), with close monitoring for hypotension. Agents used for bolus dosing include lidocaine 0.5% or bupivacaine 0.125 or 0.25%. Some clinicians use the solution of local anesthetic plus opioid prepared for continuous infusion to achieve a balance between analgesic efficacy and the adverse side effects of each agent [42]. Typical combinations are institution-specific (eg, bupivacaine 0.1 to 0.25% or ropivacaine 0.2% mixed with either fentanyl 2 to 5 mcg/mL or hydromorphone 10 to 20 mcg/mL). Some institutions include epinephrine 2 mcg/mL to enhance analgesia [43]. (See "Continuous epidural analgesia for postoperative pain: Technique and management".)

We use a mixture of 0.1% bupivacaine, fentanyl 5 mcg/mL, and epinephrine 2 mcg/mL for continuous infusion, administered at a rate of 5 to 8 mL/hour. We prefer this relatively low concentration of local anesthetic and slow infusion rate to minimize the risk of intraoperative hypotension. Some clinicians withhold the administration of epidural local anesthetic until after aortic unclamping. Release of a supraceliac cross-clamp with concomitant mesenteric traction may be followed by a period of hypotension, which would be exacerbated by sympatholysis and vasodilation produced by combinations of an epidural local anesthetic agent with a GA agent(s) [23,44]. (See 'Management of aortic unclamping' below.)

General anesthesia — GA is also used for patients undergoing open aortic surgery, either in combination with epidural analgesia or as the sole anesthetic technique.

Induction — Hypotension, hypertension, or tachycardia are avoided during and after induction of GA to minimize the risk of myocardial ischemia. In patients susceptible to developing hypotension (eg, those with diastolic dysfunction, intravascular volume depletion, or older age [≥70 years]), anesthetic agents are administered slowly or titrated in divided doses. Small doses of a vasopressor (eg, phenylephrine 40 to 200 mcg boluses) may be administered to avoid or treat hypotension during induction. For patients undergoing aneurysm repair, attempts are made to prevent sudden increases in BP due to the sympathetic response to laryngoscopy and endotracheal intubation since this increases the risk of aneurysm rupture. Thus, we typically administer a short-acting beta blocker (eg, esmolol 10 to 50 mg boluses) to avoid hypertension (and tachycardia) before laryngoscopy and intubation [45,46]. (See "Anesthesia for noncardiac surgery in patients with ischemic heart disease", section on 'Prevention of ischemia' and "Anesthesia for noncardiac surgery in patients with ischemic heart disease", section on 'Induction'.)

Maintenance — A volatile inhalation anesthetic (eg, sevoflurane, isoflurane, or desflurane) is typically used as the primary agent to maintain GA [1,2]. An advantage is the rapid titration of anesthetic concentration based on current hemodynamics and the degree of supplemental analgesia achieved with epidural infusion. Furthermore, volatile inhalation agents may have cardioprotective effects during cardiac surgery (see "Anesthesia for cardiac surgery: General principles", section on 'Maintenance techniques'). However, these have not been specifically demonstrated in abdominal aortic surgery [47-49]. A total IV anesthesia (TIVA) technique is a reasonable alternative if other patient-specific factors favor its use [1,50]. Typically, low doses of inhalation and IV agents are combined; this strategy may maintain hemodynamic stability by avoiding high doses of any one agent. (See "Anesthesia for noncardiac surgery in patients with ischemic heart disease", section on 'Maintenance'.)

Anticoagulation management — Unfractionated heparin (weight-based bolus) is administered for systemic anticoagulation before cross-clamping the aorta. The degree of heparin anticoagulation is typically monitored and maintained using the ACT (200 to 250), a POC contact activation test of the effects of heparin. If heparin is reversed with protamine, mild to moderate vasodilation or, rarely, anaphylaxis requiring emergency treatment may occur (table 4). (See "Open surgical repair of abdominal aortic aneurysm", section on 'Anticoagulation and reversal' and "Protamine reversal of heparin anticoagulation after cardiopulmonary bypass", section on 'Adverse effects of protamine: Recognition and management'.)

Hemodynamic management — Systolic and mean BP are typically maintained within 20 percent of the patient's baseline. Patients undergoing open abdominal aortic surgery are likely to develop hemodynamic instability during specific periods of the procedure due to:

●Sympathetic stimulation with hypertension during induction and endotracheal intubation, and emergence and extubation – (See 'Induction' above and 'Emergence and extubation' below.)

●Vasodilation with hypotension due to anesthetic agents, particularly the combined effects of epidural and general anesthetic agents – (See 'Anesthetic management' above.)

●Aortic cross-clamping causing a sudden increase in systolic BP and hypertension – (See 'Management of aortic cross-clamping' below.)

●Aortic unclamping, which causes a sudden decrease in systemic vascular resistance (SVR) and hypotension – (See 'Management of aortic unclamping' below.)

●Blood loss with hypovolemia causing hypotension – (See 'Fluid and transfusion management' below and "Intraoperative fluid management", section on 'Hypovolemia'.)

Hypotension may result in insufficient myocardial, cerebral, and kidney perfusion, while severe hypertension may cause myocardial ischemia, increased surgical bleeding, or aneurysm rupture. Both hypotension and hypertension are avoided or promptly treated. (See "Hemodynamic management during anesthesia in adults", section on 'Hypotension: Prevention and treatment' and "Hemodynamic management during anesthesia in adults", section on 'Hypertension: Prevention and treatment'.)

Vasoactive and other agents — Vasoactive drugs, including sympathomimetics, vasoconstrictors, vasodilators, adrenergic antagonists, and antiarrhythmics, should be readily available throughout the perioperative period to rapidly treat hypotension, hypertension, tachycardia, bradycardia, or arrhythmias.

We suggest that bolus doses of the following drugs be immediately available (table 5 and table 6):

●Vasopressors and inotropes – Phenylephrine, ephedrine, norepinephrine, vasopressin

●Vasodilators and adrenergic antagonists – Esmolol, labetalol, nitroglycerin

●Anticholinergic agent – Atropine (administered as 0.2 to 0.4 mg boluses to treat bradycardia)

In addition, we ensure immediately available infusions of vasopressor/inotropic agents (eg, phenylephrine and norepinephrine), as well as a vasodilator agent (eg, nitroglycerin).

We do not administer diuretics (eg, mannitol, furosemide) or dopamine to protect the kidneys. (See "Possible prevention and therapy of ischemic acute tubular necrosis", section on 'Experimental and unproven measures for the prevention of ischemic ATN'.)

Management of aortic cross-clamping — Application of the AXC causes a sudden increase in SVR and BP due to the sudden cessation of aortic flow and increase in LV afterload (figure 4) [51]. Stroke volume and cardiac output (CO) may decrease if myocardial dysfunction develops [22,23]. Preload is typically increased due to volume redistribution. These changes may result in myocardial ischemia detected with ECG or TEE changes, particularly in patients with coronary artery disease. (See 'Transesophageal echocardiography' above.)

Hemodynamic aberrations occurring with AXC application are not always severe and do not necessarily require aggressive treatment. The degree of pre-existing aortic occlusion and adequacy of periaortic collateral formation influence severity such that clamping an artery that is already occluded may have minimal effects. The level of clamping is also a factor. With lower-level infrarenal clamping, blood volume shifts into the splanchnic vasculature, thereby limiting increases in preload, while higher-level supraceliac clamping may cause marked increases in both preload and LV afterload, resulting in decreased LV ejection fraction (figure 5) [23,51].

After application of the AXC, therapeutic interventions are necessary for unacceptable increases in systolic BP (ie, >180 mmHg), evidence of myocardial ischemia, or LV failure due to increased afterload and preload. These may include:

●The administration of an epidural bolus of local anesthetic or increasing the epidural infusion to produce a sympathectomy, although several minutes may be required to achieve the peak effect.

●Increasing the concentration of volatile inhalation anesthetic agent to produce greater vasodilation.

●Infusion of a pharmacologic vasodilator, if necessary (table 6):

•For patients with ECG or TEE changes indicating ischemia, nitroglycerin is selected and administered as a bolus or infusion.

•For patients with severe hypertension, an arterial vasodilator such as nitroprusside or nicardipine may be selected to reduce LV afterload.

Vasodilating agents are administered in low initial doses with careful upward titration since visceral and spinal cord perfusion depends on the collateral flow below the AXC. Thus, excessive decreases in perfusion pressure are avoided. In some patients with pre-existing hypertension, it may be acceptable to allow systolic BP to remain as high as 180 mmHg while the aorta is clamped unless this results in myocardial ischemia detected by ECG changes or RWMAs on TEE imaging. (See 'Intravascular monitors' above.)

Management of aortic unclamping — Restoration of flow (eg, by removal of the ACX) results in a sudden decrease in SVR and hypotension (figure 6) [51]. This is due to the reperfusion syndrome, with hypoxia-mediated reactive hyperemia and metabolic (lactic) acidosis [51,52]. Preload is decreased due to venodilation, and myocardial contractility is reduced due to acidosis [22]. Hypotension may be profound after prolonged clamping, particularly if the clamp was applied at the suprarenal or supraceliac level. Also, metabolic acidosis and washout of ischemic muscle tissue may result in hyperkalemia, malignant arrhythmias, and cardiac arrest.

These effects may be mitigated by increasing intravascular volume near the end of the period of cross-clamping, including transfusion of salvaged or allogeneic blood if hemoglobin is ≤8 to 9 mg/dL. The anesthesiologist can work with the surgeon to allow the removal of the aortic cross clamps in most cases without the need for vasopressor agents. The surgeon can partially or intermittently remove the clamp to maintain systolic BP >90 mmHg as intravascular volume is restored. If hypotension ensues, adjusting (or reapplying) the aortic clamp can be done. If these maneuvers are unsuccessful, a bolus dose of a vasopressor can be administered, followed by continuous infusion of a vasopressor or inotropic agent (table 5).

Metabolic acidosis is treated with hyperventilation (ie, increasing the respiratory rate). When the iliac or femoral arteries are controlled independently, the distal unclamping process can be staged (ie, unclamping one side at the time) to mitigate the effects of the reperfusion syndrome. Refractory hypotension may necessitate reapplication of the AXC while hypovolemia, vasodilation, and metabolic acidosis are aggressively treated.

Before restoration of flow, blood samples for POC testing are obtained to facilitate treatment of anemia, hypoxemia, hypercarbia, acidosis, hyperkalemia, hyperglycemia, and disorders of hemostasis. Additional samples are obtained a few minutes after the AXC is released.

Fluid and transfusion management

Goal-directed fluid therapy — Since invasive monitoring is routine during major aortic surgery (eg, intra-arterial pressure monitoring and TEE) (see 'Monitoring' above), we use dynamic hemodynamic parameters to guide goal-directed fluid therapy. These include changes in LV cavity size on TEE (movie 1), and respirophasic variation in the intra-arterial pressure waveform during positive pressure ventilation (figure 1). These dynamic parameters are generally more informative than static parameters (urine output or CVP), as explained separately. (See "Intraoperative fluid management", section on 'Dynamic parameters to assess volume responsiveness' and "Intraoperative fluid management", section on 'Goal-directed fluid therapy'.)

Fluid challenges of 250 to 500 mL of a balanced crystalloid solution (eg, Ringer's lactate solution or Hartmann's solution) are administered to maintain or restore euvolemia [53]. Fluid responsiveness (ie, improvement in cardiac index with IV fluids) is suggested by TEE decreases in LV cavity size or respirophasic systolic pressure variations in the arterial waveform that exceed 15 percent. We also replace sensible and insensible losses with crystalloid infused at 0.5 to 1 mL/kg/hour [54,55]. The goal is to maintain normovolemia and optimal CO. Randomized trials in patients undergoing abdominal aortic surgery have noted a higher stroke volume index in patients receiving such goal-directed therapy (GDT) compared with a conventional approach, but no improvements in length of stay in the intensive care unit (ICU) or hospital [56,57]. (See "Intraoperative fluid management", section on 'Goal-directed fluid therapy'.)

We do not administer additional fluid solely to increase urine output (UO) since this may lead to fluid overload. Although intraoperative oliguria or anuria frequently occurs during the period of AXC, this does not predict the development of postoperative acute tubular necrosis (ATN) and acute kidney injury (AKI) [58,59]. If UO is <0.5 mL/kg per hour before aortic cross-clamping or restoring perfusion, potential causes are assessed and treated. For example, evidence of hypovolemia is treated with the administration of fluid challenges, while evidence of ventricular dysfunction is treated by initiating infusion of an inotropic agent. However, we tolerate UO <0.5 mL/kg/hour if the patient is hemodynamically stable and other monitors indicate normovolemia (eg, normal TEE cavity size and minimal respirophasic variation in the intra-arterial pressure waveform), as well as adequate cardiac function (eg, absence of TEE evidence of ventricular dysfunction) [60]. Generally, UO is restored by the end of the procedure if dynamic parameters are continuously assessed to maintain normovolemia and adequate CO throughout the intraoperative period [58,61].

We rarely use a colloid solution for a GDT bolus or any other reason (eg, replacement of blood loss). The safety and efficacy of both albumin and synthetic colloids (eg, hydroxyethyl starch [HES]) are controversial [62-64]. Although many studies evaluating GDT have used colloid boluses to maintain optimal intravascular volume, a 2010 systematic review of patients undergoing open abdominal aortic surgery noted that no single fluid type affected any outcome measure (38 trials; 1589 participants) [65]. (See "Intraoperative fluid management", section on 'Choosing fluid: Crystalloid, colloid, or blood'.)

Blood salvage and transfusion — We use an intraoperative blood salvage system (commonly referred to as a "cell saver") to minimize the need for allogeneic blood [66-68]. Details regarding the use of this technique are available in a separate topic. (See "Surgical blood conservation: Intraoperative blood salvage".)

Mean blood loss during open AAA repair is approximately 1000 mL [69]. We use standard hemoglobin thresholds (7 to 8 g/dL) unless there is evidence of ongoing bleeding or cardiac or other end-organ ischemia, in which case we transfuse for hemoglobin ≤9 g/dL. If available, we use salvaged blood first rather than relying solely on transfusion of allogeneic blood [70-73]. Also, in cases with rapid blood loss or significant ongoing bleeding, transfusion may be necessary before a quantitative laboratory assessment of hemoglobin can be obtained. These decisions are discussed in detail separately. (See "Intraoperative transfusion and administration of clotting factors", section on 'Red blood cells' and "Indications and hemoglobin thresholds for RBC transfusion in adults", section on 'Overview of our approach'.)

If ongoing bleeding is significant and unlikely to be quickly and adequately controlled (ie, the requirement for four or more units of red blood cells [RBCs] over one hour), we transfuse blood products in a 1:1:1 ratio of RBCs, fresh frozen plasma (FFP), and platelets (one unit of apheresis platelets is equivalent to six units of non-apheresis [ie, random donor or whole-blood derived] platelets) [70,73]. (See "Massive blood transfusion", section on 'Component ratio (1:1:1)'.)

In such cases, we intermittently measure hemoglobin levels and POC tests of hemostasis (eg, thromboelastography [TEG] or rotational thromboelastometry [ROTEM]) if available, as well as prothrombin time, activated partial thromboplastin time, platelet count, and fibrinogen level. (See "Intraoperative transfusion and administration of clotting factors", section on 'Point-of-care tests' and "Point-of-care hemostasis testing (viscoelastic tests)".)

Temperature management — It is essential to use warming devices, warm all IV fluids during administration, and, in some cases, increase ambient room temperature to maintain normothermia (temperature ≥35.5°C) during the intraoperative and postoperative periods. Hypothermia results in sympathetic stimulation, increases in metabolic rate and myocardial oxygen consumption, and possible ischemia development, particularly if shivering occurs. In one review of patients undergoing abdominal aortic aneurysm repair (seven studies; 765 patients), patients who developed intraoperative or postoperative hypothermia of varying degrees had a higher incidence of organ dysfunction and mortality, as well as longer hospital stays, compared with well-maintained normothermic patients [74]. Causes, consequences, and prevention of perioperative hypothermia are discussed separately. (See "Perioperative temperature management", section on 'Intraoperative hypothermia' and "Perioperative temperature management", section on 'Postoperative temperature derangements'.)

However, the lower body forced-air warmer is turned off during aortic cross-clamping to minimize oxygen (O₂) consumption and the potential for skin or muscle damage, while the lower body and extremities distal to the clamp are hypoperfused [74,75].

Ventilation management — We use a lung-protective ventilation strategy with either a volume- or pressure-limited mode of ventilation. Lung-protective strategies are particularly important for patients with chronic obstructive pulmonary disease (COPD). Further details are available elsewhere. (See "Mechanical ventilation during anesthesia in adults", section on 'Lung protective ventilation during anesthesia' and "Anesthesia for patients with chronic obstructive pulmonary disease", section on 'Mechanical ventilation'.)

Arterial blood gases are intermittently sampled (approximately every 60 minutes) if there is a significant gradient between arterial CO₂ (PaCO₂) tension and end-tidal CO₂ (ETCO₂) due to COPD. This gradient may be exacerbated during aortic cross-clamping due to decreased cardiac output. After removal of the AXC, transient metabolic acidosis is treated with hyperventilation, and PaCO₂ and pH are monitored with arterial blood gas sampling every 30 minutes until acidosis is resolved.

Emergence and extubation — Most patients undergoing elective open abdominal aortic surgery will undergo tracheal extubation in or shortly after leaving the operating room when surgery is complete [75].

In some patients, extubation may not be feasible due to failure to meet standard extubation criteria, hemodynamic instability, hypothermia (temperature <35.5°C), coagulopathy, or uncorrected hypoxemia, hypercarbia, or acidosis. These patients are transported to the ICU for postoperative controlled ventilation. (See "Extubation management in the adult intensive care unit".)

POSTOPERATIVE PAIN MANAGEMENT

Thoracic epidural analgesia — We prefer thoracic epidural analgesia (TEA) for postoperative pain management.

●Techniques – The epidural catheter is typically inserted in the immediate preoperative period or in the operating room before induction and may be used to supplement general anesthesia (GA) in the intraoperative period (see 'Epidural anesthesia' above). If the epidural catheter is not dosed during surgery, it should be activated at least 30 minutes before the end of surgery by beginning continuous epidural infusion of the postoperative analgesic agents (typically a combination of a local anesthetic and an opioid infused at 4 to 10 mL/hour). During and immediately after emergence from anesthesia, additional incremental 2 mL boluses of local anesthetic may be administered, up to 10 mL, if the patient is experiencing pain. The patient must be monitored closely for hypotension during administration of bolus doses. (See "Continuous epidural analgesia for postoperative pain: Technique and management".)

In the postoperative period, we use a continuous infusion of a mixture containing an opioid and a local anesthetic to achieve a balance between analgesic efficacy and the adverse side effects of each agent [42]. Specific combinations of local anesthetics and opioids vary according to institution or clinician preferences. Examples are a local anesthetic such as bupivacaine 0.1 to 0.25% or ropivacaine 0.2%, mixed with an opioid such as fentanyl 2 to 5 mcg/mL or hydromorphone 10 to 20 mcg/mL. Epinephrine 2 mcg/mL may be added to the selected mixture to enhance analgesia [43]. The initial postoperative epidural infusion rate is 6 mL/hour, with adjustments as needed to control pain (range 4 to 12 mL/hour). Rates are decreased for older adults (≥70 years), who require approximately 40 percent less epidural solution per hour [76]. These dilute solutions of local anesthesia allow assisted ambulation and do not commit a patient to bed rest.

Another option is patient-controlled epidural analgesia (PCEA), which allows the patient to self-administer a bolus of epidural medication with or without a basal infusion. (See "Continuous epidural analgesia for postoperative pain: Technique and management", section on 'Mode of drug delivery'.)

If continuous epidural infusion or PCEA is inadequate, an alternative approach is to split the epidural infusion by using only local anesthetic in the continuous epidural infusion, with the administration of an opioid via intravenous patient-controlled analgesia (PCA). (See "Continuous epidural analgesia for postoperative pain: Technique and management", section on 'Inadequate analgesia'.)

Typically, we continue epidural analgesia for at least three postoperative days.

●Benefits – In addition to attenuating responses to painful stimuli if used during the intraoperative period (see 'Epidural anesthesia' above), epidural analgesia provides excellent pain relief during the postoperative period. In a 2016 systematic review of 15 trials that included 1498 patients undergoing open abdominal aortic surgery, postoperative epidural analgesia after GA provided superior pain relief for up to three days compared with systemic opioid-based analgesia after GA (mean pain scores in the TEA group were 1.8 points lower on a 10 point scale) [12]. Other benefits of epidural analgesia included reduced risk of myocardial infarction (4 versus 8 percent; risk ratio [RR] 0.54, 95% CI 0.30-0.97; seven studies with 851 participants), respiratory failure (20 versus 32 percent; RR 0.69, 95% CI 0.56-0.85; six studies with 861 participants), and gastrointestinal bleeding (0.4 versus 4.0 percent; odds ratio [OR] 0.20, 95% CI 0.06-0.65; four studies with 487 participants), as well as reductions in mean time to tracheal extubation (36 hours) and time spent in the intensive care unit (six hours). Mortality rates were similar in both groups [12].

●Risks – Hypotension or an unacceptable degree of motor block may occasionally occur, warranting a change in the epidural local anesthetic or infusion rate, while respiratory depression, nausea, or severe pruritus may warrant a change in the epidural opioid. Rarely, other adjuvants may be administered via epidural infusion in combination with local anesthetics. Details regarding these alternatives are available elsewhere. (See "Continuous epidural analgesia for postoperative pain: Technique and management", section on 'Monitoring during epidural analgesia'.)

Complications of epidural analgesia include spinal epidural hematoma (SEH), which is more frequent in the setting of vascular surgery (1 in 1000 patients) compared with other types of surgery, perhaps due to intraoperative systemic anticoagulation [77]. The risk of SEH increases if the patient has impaired coagulation at the time of placement or removal of the epidural catheter; thus, the timing of epidural placement and removal is carefully coordinated with intraoperative anticoagulation and reversal, as well as with perioperative antithrombotic prophylaxis. (See "Neuraxial anesthesia/analgesia techniques in the patient receiving anticoagulant or antiplatelet medication".)

Vascular surgery patients also have a higher incidence of epidural abscess (1 in 4000 patients) compared with those undergoing other types of surgery, perhaps due to older age, a higher incidence of diabetes and chronic kidney disease, longer duration of postoperative epidural analgesic administration, and higher risk of developing infected SEH [77,78]. Overall, complications of epidural placement are rare and are discussed separately. (See "Spinal epidural abscess" and "Neuraxial anesthesia/analgesia techniques in the patient receiving anticoagulant or antiplatelet medication", section on 'Prevention of neurologic damage from spinal hematoma'.)

Alternative and supplemental techniques for postoperative analgesia — For some patients, neither thoracic nor lumbar epidural analgesia is appropriate due to coagulopathy, anatomic considerations, patient refusal, or emergency surgery. Attempts to place an epidural catheter may occasionally be unsuccessful. Other options to consider for such patients include:

●Patient-controlled analgesia (PCA) with systemic opioids – The most common alternative technique is the administration of IV systemic opioids via PCA, typically employed as part of a multimodal strategy that includes nonopioid analgesic agents or regional techniques [79-81]. For example, a transverse abdominis plane (TAP) block may be performed to provide partial relief [82]. (See "Use of opioids for acute pain in hospitalized patients" and "Thoracic paravertebral block procedure guide" and "Transversus abdominis plane (TAP) blocks procedure guide".)

●Paravertebral block (PVB) – Placement of a PVB may be useful in some instances but would not be placed if coagulopathy is present [83,84]. (See "Thoracic paravertebral block procedure guide" and "Neuraxial anesthesia/analgesia techniques in the patient receiving anticoagulant or antiplatelet medication".)

●Transverse abdominis plane (TAP) block – The TAP block can provide effective analgesia for large abdominal incisions, particularly retroperitoneal incisions [85]. The continuous TAP block is a fascial plane block (ie, not a neuraxial block) performed by placing a catheter to administer local anesthetic in the plane between transversus abdominis and internal oblique muscles. (See "Transversus abdominis plane (TAP) blocks procedure guide".)

●Intrathecal morphine – This may considered as a supplementary alternative to improve postoperative analgesia in some patients if a spinal anesthesia technique is feasible [86]. (See "Spinal anesthesia: Technique".)

Further details regarding the management of acute postoperative pain are discussed separately. (See "Approach to the management of acute pain in adults".)

EMERGENCY AORTIC SURGERY — 

Emergency open aortic surgery is generally necessary to manage aortic rupture from any cause and may be needed to manage acute aortic occlusion. Even when control of hemorrhage is initially attempted or successfully achieved by an endovascular method, definitive repair with open aortic surgery may be necessary. Details regarding the initial evaluation and surgical management of these emergencies can be found in the following topics:

●(See "Open surgical repair of abdominal aortic aneurysm".)

●(See "Surgical and endovascular repair of ruptured abdominal aortic aneurysm".)

●(See "Surgical and endovascular management of acute type B aortic dissection".)

●(See "Overview of damage control surgery and resuscitation in patients sustaining severe injury" and "Overview of damage control surgery and resuscitation in patients sustaining severe injury", section on 'Damage control laparotomy' and "Abdominal vascular injury", section on 'Abdominal aorta'.)

Preparation — The following equipment and medications are prepared upon notice that a patient will require urgent or emergency surgery. Typically, it is necessary to have at least one assistant for these preparations, which may continue even after the patient arrives arrival of the patient in the operating room.

●Monitors – Equipment for insertion of the intra-arterial catheter, central venous access, and transesophageal echocardiogram (TEE) is prepared in advance, if feasible. However, in a hemodynamically unstable patient, induction of anesthesia and initiation of emergency surgery should not be delayed; these monitors may be inserted postinduction when necessary.

●Vasoactive drugs – Vasoactive drugs should be prepared in advance, if feasible, since the need for emergency treatment of hypotension, hypertension, tachycardia, bradycardia, and arrhythmias is likely. (See 'Vasoactive and other agents' above.)

●Preparation for transfusion – Typing and crossmatching for at least 10 units of red blood cells (RBCs) and fresh frozen plasma (FFP) or similar products (eg, plasma frozen within 24 hours of collection [PF24]) is performed for cases of aortic rupture. The blood bank should be alerted to the potential need for massive transfusion. (See "Surgical and endovascular repair of ruptured abdominal aortic aneurysm", section on 'Preparation'.)

High-volume transfusion and warming devices for fluid and blood administration are prepared since significant blood loss is likely (see 'Blood salvage and transfusion' above). Other body-warming devices (eg, forced-air warmers) are also prepared (see 'Temperature management' above). These measures are necessary to avoid hypothermia and hypothermic coagulopathy during rapid transfusion in a patient with an open abdominal cavity. (See "Massive blood transfusion", section on 'Complications'.)

Evaluation and preoperative management

●A rapid preanesthesia evaluation is performed, similar to that for emergency cardiac surgery. (See "Overview of preoperative evaluation and management for cardiac surgery in adults", section on 'Emergency surgery'.)

●Two large-bore peripheral intravenous catheters should be inserted immediately to administer medications, fluids, and, if necessary, blood transfusions. Although materials for placement of central venous access are prepared in advance (see 'Preparation' above), these are frequently inserted after anesthetic induction.

●An intra-arterial catheter is inserted as soon as feasible to continuously monitor blood pressure (BP). (See 'Intravascular monitors' above.)

●Intravenous analgesics are administered in patients with symptomatic abdominal aortic aneurysm (AAA) for control of abdominal, back, or flank pain, but consciousness should be maintained until the time of induction.

●In patients with hypertension, a short-acting IV beta blocker such as esmolol may be administered as intermittent boluses or as an infusion to control BP when necessary. A relatively low systolic BP (80 to 100 mmHg) is allowed during emergency preoperative imaging studies and transport to the operating room. Vasopressors and inotropes are administered with caution in the preoperative period to avoid further aortic rupture with exacerbation of bleeding. (See "Surgical and endovascular repair of ruptured abdominal aortic aneurysm", section on 'Preparation'.)

Induction of general anesthesia — Severe hypotension may occur during induction of general anesthesia (GA). Thus, surgical prepping and draping are completed before administering anesthetic induction agents. For patients who are hemodynamically unstable due to intrabdominal hemorrhage, the aortic cross-clamp (AXC) is applied soon after the abdomen has been entered. Some surgeons may deploy an endovascular balloon to occlude the aorta as a temporary measure to increase BP to allow for controlled anesthetic induction. (See "Surgical and endovascular repair of ruptured abdominal aortic aneurysm", section on 'Preoperative balloon occlusion'.)

Rapid sequence induction is typically necessary (see "Rapid sequence induction and intubation (RSII) for anesthesia"). We use etomidate or ketamine as the primary induction agent due to their favorable hemodynamic profile, and we avoid or reduce the doses of adjuvant agents to minimize hypotension. An alternative induction technique is to administer a relatively high dose of opioid (eg, fentanyl 5 to 8 mcg/kg) together with a reduced dose of an IV induction agent. (See "General anesthesia: Intravenous induction agents".)

For patients who remain hypertensive at the time of induction (eg, impending or contained aortic rupture in a hypertensive patient), we avoid further increases in BP by administering one or more adjuvant agents (eg, an opioid or lidocaine) together with the primary induction agent, to blunt airway reflexes and the sympathetic stress response to laryngoscopy and endotracheal intubation. (See "General anesthesia: Intravenous induction agents", section on 'Adjuvant agents'.)

Maintenance of anesthesia is similar to that for elective procedures. (See 'Maintenance' above.)

Fluid and blood management — Hemodynamic monitoring and management are similar to elective aortic repair. However, hemodynamic instability is typically more dramatic during emergency surgery for aortic rupture or acute aortic occlusion. (See 'Intravascular monitors' above and 'Hemodynamic management' above.)

We avoid aggressive administration of fluids or RBCs before AXC application to avoid dilutional coagulopathy [87,88]. After AXC application, blood products are transfused as necessary in a 1:1:1 ratio of RBCs, FFP, and platelets. (See 'Blood salvage and transfusion' above.)

Hemodynamic management — In the absence of randomized controlled trials, the goal of hemodynamic management is to maintain normotension (ie, systolic BP >100 mmHg); fluids and vasopressor agents are administered as necessary [88]. Some centers allow a lower systolic BP target of 50 to 100 mmHg without evidence of poor perfusion (called permissive hypotension), although data supporting this practice are scant [88,89].

Postoperative management — After emergency open aortic surgery, most patients remain intubated and sedated with controlled ventilation. A pain control regimen suitable for critically ill patients is used. (See "Pain control in the critically ill adult patient".)

SOCIETY GUIDELINE LINKS — 

Links to society and government-sponsored guidelines from selected countries and regions worldwide are provided separately. (See "Society guideline links: Aortic and other peripheral aneurysms" and "Society guideline links: Aortic dissection and other acute aortic syndromes".)

SUMMARY AND RECOMMENDATIONS

●Preanesthesia consultation – The preanesthesia consultation focuses on assessing and minimizing cardiovascular, pulmonary, and renal risks and planning for postoperative analgesia. (See 'Preanesthetic consultation' above.)

●Monitoring

•An intra-arterial catheter is inserted to continuously monitor arterial blood pressure (BP), evaluate respirophasic variations in the arterial pressure waveform (figure 1), and perform intermittent blood sampling. Also, a sheath introducer (eg, Cordis) can be inserted to administer vasoactive drug infusions, monitor central venous pressure (CVP), and provide large-bore venous access for fluid and blood administration. (See 'Intravascular monitors' above.)

•Transesophageal echocardiography (TEE) is used to avoid hypovolemia or hypervolemia, monitor for regional and global ventricular dysfunction (figure 2 and figure 3), assess causes of hypotension, and detect air or particulate emboli or aortic pathology (eg, dissection). (See 'Transesophageal echocardiography' above.)

●Anesthetic management – We suggest an intraoperative anesthetic technique that combines general anesthesia (GA) and thoracic epidural analgesia (TEA) rather than GA alone (Grade 2C). The addition of epidural anesthesia during GA attenuates responses to painful stimuli related to the typically large incisions and reduces intraoperative anesthetic and opioid dosing. (See 'Anesthetic management' above.)

•Epidural anesthesia – The epidural catheter is typically inserted before anesthetic induction. To minimize the risk of spinal epidural hematoma, the timing for epidural catheter placement and removal is carefully coordinated with the administration of antithrombotic prophylactic medications and planned intraoperative heparin. Intraoperative use of epidural anesthesia, in addition to GA, attenuates responses to painful stimuli, allowing reduction of anesthetic and opioid dosing, and may facilitate early extubation in or shortly after leaving the operating room. Combinations of local anesthetic plus an opioid achieve a balance between analgesic efficacy and adverse side effects of each agent. (See 'Epidural anesthesia' above.)

•General anesthesia – Hypotension, hypertension, or tachycardia are avoided during and after induction of GA to minimize the risk of myocardial ischemia. A volatile inhalation anesthetic (eg, sevoflurane, isoflurane, or desflurane) is typically used as the primary agent to maintain GA, although total intravenous anesthesia (TIVA) is an acceptable alternative. (See 'General anesthesia' above.)

●Fluid and blood management – Since invasive monitoring is routine during major aortic surgery (eg, intra-arterial pressure monitoring and TEE) (see 'Monitoring' above), dynamic hemodynamic parameters guide goal-directed fluid therapy. These include changes in left ventricular (LV) cavity size on TEE (movie 1), and respirophasic variation in the intra-arterial pressure waveform during positive pressure ventilation (figure 1). These dynamic parameters are generally more informative than static parameters (urine output or CVP). (See 'Goal-directed fluid therapy' above.)

Intraoperative blood salvage is used to minimize the need for allogeneic blood transfusion in open abdominal aortic procedures as in other major surgeries with the potential for substantial blood loss. This is discussed in detail separately. (See "Surgical blood conservation: Intraoperative blood salvage".)

Standard hemoglobin thresholds for transfusion are used (7 to 8 g/dL) unless there is evidence of ongoing bleeding or cardiac or other end-organ ischemia, in which case we transfuse for hemoglobin ≤9 g/dL. These decisions are discussed in detail separately. (See "Intraoperative transfusion and administration of clotting factors", section on 'Red blood cells' and "Indications and hemoglobin thresholds for RBC transfusion in adults", section on 'Overview of our approach'.)

●Hemodynamic management – Hemodynamic changes often require specific management during aortic cross-clamp (AXC) application (figure 4 and figure 5) and removal (figure 6). Vasopressors, inotropic agents, and vasodilators are prepared in advance and immediately available (table 5 and table 6). (See 'Hemodynamic management' above.)

●Temperature management – Normothermia (temperature ≥35.5°C) is maintained using devices for warming the upper and lower body and all IV fluids and blood. However, the lower body forced-air warmer is turned off when the aorta is cross-clamped to minimize the potential for skin or muscle damage while the lower body is hypoperfused. (See 'Temperature management' above.)

●Ventilation management – As discussed separately, a lung-protective ventilation strategy is used (see "Mechanical ventilation during anesthesia in adults", section on 'Lung protective ventilation during anesthesia'). After removal of the AXC, hyperventilation can be provided to compensate for transient metabolic acidosis. (See 'Ventilation management' above.)

●Postoperative pain management – We recommend continuous TEA for the management of postoperative pain rather than using systemic opioid-based analgesia alone (Grade 1B). Postoperative TEA provides optimal pain relief for the extensive incisions used for open abdominal aortic surgery and also reduces the risk of postoperative pneumonia, respiratory failure, and myocardial infarction. (See 'Postoperative pain management' above.)

●Emergency aortic surgery – Some aspects of anesthetic management are modified for emergency aortic surgery (see 'Emergency aortic surgery' above):

•Preparation – At least one assistant is necessary to prepare monitors, vasoactive drugs, high-volume transfusion devices, and warming devices. (See 'Preparation' above.)

•Preoperative management – Two large-bore peripheral IV catheters are immediately inserted to administer medications, fluids, and blood. Any central venous access is frequently inserted after anesthetic induction. An intra-arterial catheter is inserted as soon as feasible to continuously monitor BP. (See 'Intravascular monitors' above.)

•Induction – Rapid sequence induction is typically necessary (see "Rapid sequence induction and intubation (RSII) for anesthesia"). Because severe hypotension may occur during the induction of GA, etomidate or ketamine is typically selected as the primary induction agent due to its favorable hemodynamic profile, and doses of adjuvant agents are reduced or avoided. Furthermore, surgical prepping and draping is completed before administering anesthetic induction agents. The AXC may be applied soon after the abdomen has been entered; an alternative strategy is deploying an endovascular balloon to occlude the aorta and increase BP. (See 'Induction of general anesthesia' above.)

•Fluid and blood management – Aggressive administration of fluids or red blood cells (RBCs) is avoided until after AXC application; then, blood products are transfused in a 1:1:1 ratio of RBCs, fresh frozen plasma (FFP), and platelets. (See 'Fluid and blood management' above.)

•Hemodynamic management – Fluids and vasopressor agents are administered as necessary to maintain normotension with a target systolic BP >100 mmHg. (See 'Hemodynamic management' above.)

•Postoperative management – Most patients remain intubated and sedated with controlled ventilation. A pain control regimen suitable for critically ill patients is used. (See "Pain control in the critically ill adult patient".)