Anesthesia for open abdominal aortic surgery

INTRODUCTION — Open aortic surgery is employed for patients who have indications for abdominal aortic aneurysm (AAA) repair but unfavorable anatomy for endovascular aortic repair. Open aortic surgery is also necessary to manage aortic thrombosis or repair of aortic rupture from any cause (eg, ruptured AAA, ruptured aortic dissection, traumatic rupture), even when control of hemorrhage is initially achieved by an endovascular method.

This topic will review anesthetic management for patients undergoing open abdominal aortic surgery. Management for endovascular aortic repair is discussed separately. (See "Anesthesia for endovascular aortic repair".)

Elective and emergency surgical repairs of the abdominal aorta are discussed in other topics:

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

●(See "Endovascular repair of abdominal aortic aneurysm".)

●(See "Management of symptomatic (non-ruptured) and ruptured abdominal aortic aneurysm".)

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

●(See "Management of acute type B aortic dissection".)

●(See "Endovascular methods for aortic control in trauma".)

PREANESTHETIC CONSULTATION — The preanesthetic consultation focuses on assessing perioperative risks and consulting with the surgeon and other specialists to ensure that risks are minimized. (See "Open surgical repair of abdominal aortic aneurysm", section on 'Preoperative evaluation' and "Management of asymptomatic abdominal aortic aneurysm", section on 'Medical risk assessment'.)

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].

A preoperative electrocardiogram (ECG) is useful as a baseline if the postoperative ECG is abnormal. Additional cardiac testing is indicated only in patients with changes in cardiac symptoms and functional status. (See "Evaluation of cardiac risk prior to noncardiac surgery".)

●Pulmonary risk – Many patients undergoing abdominal aortic surgery are current or former tobacco users with chronic obstructive pulmonary disease (COPD). Evaluation and management of preoperative pulmonary risk is discussed separately. (See "Anesthesia for patients with chronic obstructive pulmonary disease", section on 'Preanesthesia consultation' and "Evaluation of perioperative pulmonary risk" and "Strategies to reduce postoperative pulmonary complications in adults".)

●Renal risk – Open aortic repair carries a high risk for perioperative acute kidney injury (AKI) [4]. Elevated preoperative serum creatinine is the strongest predictor of postoperative renal 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 contrast or other nephrotoxins, anemia, and need for emergency surgery, particularly for ruptured abdominal aortic aneurysm (AAA) [4,8]. Intraoperative factors that may exacerbate or cause AKI include open aortic repair, suprarenal or juxtarenal aortic cross-clamping, prolonged cross-clamping, embolism of atherosclerotic debris into the renal arteries, and/or hemodynamic instability.

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

•Avoidance of preoperative, intraoperative, and postoperative anemia (See "Perioperative blood management: Strategies to minimize transfusions", section on 'Treatment of anemia'.)

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

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

•Avoidance or treatment of hypotension (See "Hemodynamic management during anesthesia in adults", section on 'Hypotension: Prevention and treatment'.)

•Avoidance or treatment of hyperglycemia (See "Glycemic control in critically ill adult and pediatric patients".)

Preoperative laboratory testing — Preoperative laboratory tests (complete blood count, tests of hemostasis, electrolytes, glucose, blood urea nitrogen [BUN], creatinine) provide baseline values for comparison with intraoperative point-of-care and postoperative tests. (See 'Point-of-care testing' below.)

Typing and crossmatching for 2 to 4 units of red blood cells (RBCs) is performed; these should be available in the operating room prior to surgical incision. (See "Open surgical repair of abdominal aortic aneurysm", section on 'Blood for transfusion'.)

Management of medications — Perioperative cardiovascular, thrombotic, and infectious complications are minimized by continuing chronic medications and managing 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'.)

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

●Prophylactic antibiotics – Administration of the selected antibiotic within the recommended timeframe is ensured (table 4).

Planning for postoperative pain management — Patients undergoing open aortic aneurysm repair have significant postoperative pain, which contributes to morbidity [10,11]. Techniques, risks, and benefits of epidural analgesia are discussed, and the patient's back is examined, during the preanesthesia consultation. (See 'Epidural anesthesia' below and 'Postoperative pain management' below.)

INTRAOPERATIVE ANESTHETIC MANAGEMENT

Epidural anesthesia

Catheter placement for postoperative analgesia — We employ continuous thoracic epidural analgesia (TEA) to achieve adequate postoperative pain control with minimal respiratory depression after open abdominal aortic surgery [11,12]. The TEA catheter is inserted in the immediate preoperative period or in the operating room shortly before induction of general anesthesia (GA), at least one hour before planned intraoperative administration of a bolus of intravenous (IV) 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 the T6 to T7 level to achieve optimal postoperative pain control [13-15], most have suggested the T9 to T12 level to attain the advantages of TEA while minimizing hemodynamic instability [12,16-18]. Higher TEA may not provide adequate analgesia caudally in patients with iliofemoral involvement, and further cephalic spread may not provide additional benefits. A lumbar epidural technique is a reasonable alternative if thoracic catheter placement is technically difficult due to anatomical considerations, and this option may be as effective for postoperative analgesia, particularly if an opioid is added to the continuous epidural infusion [19-21].

Immediately after insertion of the epidural catheter, a test dose is administered to exclude possible intravascular or intrathecal spread and to ensure that the block will be effective for intraoperative use. Typically, the test dose is 3 mL of 1.5% lidocaine with 1:200,000 epinephrine. We administer an additional 2 mL of this solution after waiting five to seven minutes, then test the level of sensory analgesia bilaterally. Loss of sensation to temperature or pinprick is commonly used to assess the extent of epidural anesthesia. Details regarding techniques for epidural catheter placement are described separately. (See "Epidural and combined spinal-epidural anesthesia: Techniques", section on 'Epidural anesthesia technique'.)

The use of TEA for postoperative pain control is discussed below. (See 'Postoperative pain management' below.)

Intraoperative use — We typically employ an intraoperative anesthetic technique that combines GA and epidural anesthesia. Addition of intraoperative epidural anesthesia/analgesia during GA attenuates responses to painful stimuli to reduce intraoperative anesthetic and opioid requirement and provides optimal pain control that may facilitate early extubation in the operating room [22,23]. Continued use of TEA in the postoperative period reduces risk of myocardial infarction, respiratory failure, and arterial graft occlusion, and facilitates early recovery of bowel function [11,15,24-28]. As noted below, TEA also provides superior postoperative pain control. (See 'Thoracic epidural analgesia' below.)

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 2% or bupivacaine 0.125 or 0.25%. Some clinicians use the solution of local anesthetic plus opioid prepared for continuous infusion. Such combinations of local anesthetic plus opioid achieve a balance between analgesic efficacy and the adverse side effects of each agent [29]. 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 [30]. (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 risk of intraoperative hypotension. Some clinicians withhold 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 epidural local anesthetic agent with general anesthetic agent(s) [31,32]. (See 'Management of aortic unclamping' below.)

Two large bore peripheral intravascular catheters (IVs) are often inserted with one attached to a fluid warmer. If a central line cordis is used, one large bore peripheral IV may provide adequate additional vascular access.

General anesthesia — GA is selected for most patients undergoing open aortic surgery, either as the sole anesthetic technique or in combination with TEA. In rare circumstances (eg, severe pulmonary impairment in patients who are not candidates for endovascular aortic repair), a neuraxial technique may be used without GA for open abdominal aortic surgery [33,34].

Induction — Techniques for GA should minimize risk of myocardial ischemia. (See "Anesthesia for noncardiac surgery in patients with ischemic heart disease", section on 'Prevention of ischemia'.)

A reasonable approach is induction with a short-acting hypnotic (eg, etomidate 0.3 mg/kg or a low dose of propofol [approximately 1 mg/kg] administered slowly) combined with a moderate dose of an opioid (eg, fentanyl 1 to 2 mcg/kg) and/or lidocaine 50 to 100 mg to blunt the sympathetic and airway responses to laryngoscopy and intubation. A muscle relaxant is administered to facilitate laryngoscopy.

In patients susceptible to developing hypotension (eg, older age [≥70 years], intravascular volume depletion, diastolic dysfunction), 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.

Conversely, patients who develop marked hypertension due to the sympathetic response to laryngoscopy and endotracheal intubation are at risk of aortic aneurysm rupture. For this reason, we typically administer a short-acting beta blocker (eg, esmolol 10- to 50-mg boluses) to avoid or treat hypertension and tachycardia during intubation [35,36]. (See "Anesthesia for noncardiac surgery in patients with ischemic heart disease", section on 'Induction'.)

Maintenance — In most patients, we prefer a volatile inhalation anesthetic (eg, sevoflurane, isoflurane, or desflurane) as the primary agent to maintain GA [1,2]. An advantage is rapid titration of anesthetic concentration based on current hemodynamics and the degree of analgesia achieved with epidural infusion. While these agents may have cardioprotective effects, this has not been demonstrated in abdominal aortic surgery [37-39]. A total IV anesthesia (TIVA) technique is a reasonable alternative if other patient-specific factors favor its use [1,40]. (See "Anesthesia for noncardiac surgery in patients with ischemic heart disease", section on 'Maintenance'.)

Nitrous oxide (N₂O) is avoided since it causes bowel distension and increases risk for postoperative nausea and vomiting (PONV) [41-43]. (See "Maintenance of general anesthesia: Overview", section on 'Nitrous oxide gas'.)

Monitoring

Standard monitoring — All patients have standard noninvasive monitoring, including electrocardiography (ECG), pulse oximetry (SpO₂), and intermittent noninvasive blood pressure (NIBP) cuff measurements (table 5).

We use continuous ECG monitoring with leads II and V₅, with computerized ST-segment trending to detect myocardial ischemia and/or arrhythmias. Multiple-lead monitoring is more sensitive than single-lead monitoring, and computerized ST-segment analysis is superior to visual clinical interpretation for identification of ischemic ST-segment changes. (See "Anesthesia for noncardiac surgery in patients with ischemic heart disease", section on 'Monitoring for myocardial ischemia'.)

End-tidal carbon dioxide (ETCO₂) and airway pressures and volumes are continuously monitored after endotracheal intubation.

An intra-arterial catheter is always inserted (see "Intra-arterial catheterization for invasive monitoring: Indications, insertion techniques, and interpretation"), ideally before anesthetic induction. Patients with abdominal aortic aneurysm (AAA) often have peripheral arterial atherosclerosis and discrepancies in blood pressure (BP) between right and left upper extremities. Ultrasound guidance can facilitate catheterization of the radial artery. (See "Intra-arterial catheterization for invasive monitoring: Indications, insertion techniques, and interpretation", section on 'Use of ultrasound guidance'.)

The intra-arterial catheter is used for:

●Continuous monitoring of arterial BP. However, mean arterial BP is poorly correlated with cardiac index [44].

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

●Intermittent blood sampling. (See 'Point-of-care testing' below.)

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

A central venous catheter (CVC) is often inserted to provide large-bore venous access for fluid and blood administration and for vasoactive drug infusions. Use of a pulmonary artery catheter (PAC) is rare but may be helpful in the setting of severe right ventricular (RV) dysfunction or severe pulmonary hypertension. In patients with a CVC or PAC, 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 prefer transesophageal echocardiography (TEE) 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.)

Specifically, 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 ECG or PAC changes (figure 2 and figure 3). Although there are no data demonstrating 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 causes a sudden, large increase in left ventricular (LV) systolic afterload that often leads to myocardial ischemia and/or LV failure with hemodynamic instability [31,45-50]. RWMAs may progressively worsen after placement of the aortic cross-clamp (AXC), with progression to global severe hypokinesis. TEE indicators of poor global LV systolic or diastolic function predict postoperative congestive heart failure (CHF) and/or prolonged intubation after abdominal aortic surgery [51,52]. (See 'Management of aortic cross-clamping' below.)

●Assess causes of hypotension. For example. after aortic unclamping, TEE is used to identify causes of hypotension such as decreased preload due to venodilation or myocardial dysfunction due to acidosis. (See 'Management of aortic unclamping' below.)

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

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)".)

Point-of-care testing — Point-of-care testing (POCT) during open aortic surgery typically includes arterial blood gases and pH, hemoglobin, electrolytes, glucose, and activated clotting time (ACT). Available tests of hemostasis are employed when there is evidence of coagulopathy or significant bleeding [53]. (See "Clinical use of coagulation tests", section on 'Point-of-care testing'.)

We obtain at least three sets of measurements during open aortic surgery: baseline values (after induction), during aortic cross-clamping, and after unclamping prior to extubation.

Temperature management — Warming devices are employed to maintain normothermia (temperature ≥35.5°C) [54-57]. These include upper- and lower-body forced-air warming devices and blankets, insulation water mattresses, and devices for warming all IV fluids. In some cases, it may be necessary to adjust the operating room temperature to maintain body temperature. Notably, the lower body forced-air warmer is turned off during the period of aortic cross-clamping because organs distal to the clamp may be hypoperfused and become ischemic.

Hypothermia and shivering are avoided because of potential complications (eg, coagulopathy, myocardial ischemia). 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 [58]. (See "Overview of post-anesthetic care for adult patients", section on 'Hypothermia or hyperthermia'.)

Anticoagulation management — Prior to cross-clamping the aorta during elective aortic surgery (eg, AAA repair), unfractionated heparin is administered for systemic anticoagulation. If heparin is reversed with protamine, mild to moderate vasodilation or, rarely, anaphylaxis requiring emergent treatment may occur (table 6). (See "Perioperative anaphylaxis: Clinical manifestations, etiology, and management", section on 'Initial management'.)

Fluid and transfusion management — All IV fluids are warmed to avoid hypothermia. (See 'Temperature management' above.)

Goal-directed fluid therapy — We use a goal-directed approach to fluid therapy, using dynamic parameters to assess intravascular volume status and guide fluid administration. (See "Intraoperative fluid management", section on 'Dynamic parameters to assess volume responsiveness'.)

We prefer to use TEE changes in LV cavity size (movie 1). Respirophasic variation in the intra-arterial pressure waveform during positive pressure ventilation may also be used as a primary or supplementary dynamic parameter (figure 1). Fluid responsiveness (ie, improvement in cardiac index with administration of IV fluids) is suggested by TEE decreases in LV cavity size or by respirophasic systolic pressure variations in the arterial waveform exceeding 15 percent.

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 [59]. We also replace sensible and insensible losses with crystalloid infused at a rate of 0.5 to 1 mL/kg/hour [60,61]. The goal is to maintain normovolemia and optimal cardiac output (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 [62,63]. Studies in other patient groups have noted improved clinical outcomes. (See "Intraoperative fluid management", section on 'Goal-directed fluid therapy'.)

Fluid administration solely for the purpose of increasing UO is not recommended, as this may lead to fluid overload. Although intraoperative oliguria or anuria frequently occurs during the period of aortic cross-clamping, this does not predict development of postoperative acute kidney injury (AKI) [64,65]. If UO is <0.5 mL/kg/hour before aortic cross-clamping or after aortic unclamping, potential causes are assessed and treated. For example, evidence of hypovolemia is treated with 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) [66]. 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 [64,67].

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 [68-70]. Although many studies evaluating GDT have used colloid boluses to maintain optimal intravascular volume, a 2010 systematic review in patients undergoing open abdominal aortic surgery noted that no single fluid type affected any outcome measure (38 trials; 1589 participants) [71]. (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 [72-74]. (See "Surgical blood conservation: Intraoperative blood salvage".)

Mean blood loss during open AAA repair is approximately 1000 mL [75]. We transfuse salvaged or crossmatched red blood cells (RBCs) when hemoglobin is ≤8 g/dL in patients without ischemic heart disease, in the absence of significant ongoing bleeding [76,77]. We use a higher threshold of ≤9 g/dL if a patient has severe or unstable ischemic heart disease, evidence of cardiac or other organ ischemia, or ongoing bleeding [77-80]. (See "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, requirement for 4 or more units of RBCs over one hour), we transfuse blood products in a 1:1:1 ratio of RBCs, fresh frozen plasma (FFP), and platelets (1 unit of apheresis platelets is equivalent to 6 units of non-apheresis [ie, random donor or whole-blood derived] platelets) [77,80]. (See "Massive blood transfusion", section on 'Data for specific patient populations'.)

In such cases, we intermittently measure hemoglobin levels and point-of-care 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 "Clinical use of coagulation tests", section on 'Point-of-care testing' and "Clinical use of coagulation tests", section on 'Evaluation of abnormal results'.)

Further details regarding management of severe intraoperative bleeding can be found in other topics. (See "Massive blood transfusion".)

Hemodynamic management — Systolic and mean BP are typically maintained within 20 percent of the patient's baseline. Hypotension may result in insufficient myocardial, cerebral, and renal perfusion, while severe hypertension may cause myocardial ischemia, increased surgical bleeding, or aneurysm rupture.

Patients undergoing open abdominal aortic surgery may develop hemodynamic instability due to:

●Aortic cross-clamping

●Aortic unclamping

●Blood loss with hypovolemia

●Vasodilation due to anesthetic agents, particularly the combined effects of epidural and general anesthetic agents

●Sympathetic stimulation with tracheal intubation during induction and extubation during emergence

Vasoactive drugs — 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:

●Vasopressors and inotropes – Phenylephrine, ephedrine, norepinephrine, vasopressin (table 7)

●Vasodilators and adrenergic antagonists – Esmolol, labetalol, nitroglycerin (table 8)

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

In addition, we prepare infusions of a vasopressor/inotrope (eg, phenylephrine and norepinephrine) and a vasodilator (eg, nitroglycerin) and keep these immediately available (table 7 and table 8).

Management of aortic cross-clamping — Application of the AXC causes a sudden increase in systemic vascular resistance (SVR) and BP due to the sudden impedance to aortic flow and increase in LV afterload (figure 4) [81]. Stroke volume and CO may decrease if myocardial dysfunction develops [31,45]. Preload is typically increased due to volume redistribution. These changes may result in myocardial ischemia detected with ECG and/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 preexisting aortic occlusion and adequacy of periaortic collateral formation influence severity; clamping an artery that is already occluded may have minimal affects. 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, and a resultant decrease in LV ejection fraction (figure 5) [31,81].

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

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

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

●Infusion of a pharmacologic vasodilator, if necessary (table 8):

•For patients with ECG or TEE changes indicating ischemia, nitroglycerin is selected and administered as a bolus and/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 are dependent on collateral flow below the AXC. Thus, excessive decreases in perfusion pressure are avoided. In some patients with preexisting 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 the TEE. (See 'Monitoring' above.)

To minimize oxygen (O₂) consumption of the lower body and to prevent muscle damage, the lower-body forced-air warmer is turned off during the period when the aorta is cross-clamped [82].

Management of aortic unclamping — Removal of the AXC results in a sudden decrease in SVR and hypotension (figure 6) [81]. This is due to the reperfusion syndrome, with hypoxia-mediated reactive hyperemia and metabolic (lactic) acidosis [81,83]. Preload is decreased due to venodilation, and myocardial contractility is decreased due to acidosis [45]. Hypotension may be profound after a prolonged clamping period, particularly if the AXC 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. Typically, a bolus dose of a vasopressor is administered just as the AXC is removed, followed by continuous infusion of a vasopressor or inotropic agent (table 7). Metabolic acidosis is treated with hyperventilation (ie, increasing the respiratory rate). In some cases, the unclamping process is 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 release of the AXC, blood samples for POCT are obtained to facilitate treatment of anemia, hypoxemia, hypercarbia, acidosis, hyperkalemia, hyperglycemia, and disorders of hemostasis. Additional samples are obtained a few minutes after release of the AXC.

Ventilation management — Patients undergoing open aortic surgery may benefit from lung-protective controlled ventilation [84-88], particularly those with chronic obstructive pulmonary disease (COPD). Either a volume- or pressure-limited ventilation mode may be used with:

●Low tidal volumes of 6 to 8 mL/kg predicted body weight

●Respiratory rate at 8 to 10 breaths/minute, with adequate expiratory time (ie, inspiratory-to-expiratory [I:E] ratio of 1:3) to reduce air trapping

●Maintenance of plateau pressures at <15 to 20 cmH₂O; maintenance of peak airway pressures <35 cmH₂O

●Fraction of inspired O₂ (FiO₂) adjusted to maintain O₂ saturation >92 percent

●Cautious use of positive end-expiratory pressure (PEEP) at 5 to 8 cmH₂O to keep the small airways open, with continuous monitoring for signs of hyperinflation

In a 2015 systematic review of 12 trials that included 1012 patients undergoing any type of surgery, lower tidal volumes (6 to 8 mL/kg) decreased the need for postoperative invasive ventilation (risk ratio [RR] 0.33, 95% CI 0.14-0.80) compared with higher tidal volumes (10 to 12 mL/kg) [87]. Similarly, a 2016 meta-analysis of patients undergoing any type of surgery (16 trials; 1054 patients) noted decreased incidence of postoperative lung infection for lower tidal volumes compared with higher tidal volumes (odds ratio [OR] 0.33, 95% CI 0.16-0.68) [88]. In patients undergoing major abdominal surgery, a randomized trial that included 400 patients found a higher incidence of a composite of major pulmonary and extrapulmonary complications in patients receiving the higher tidal volumes (RR 0.40, 95% CI 0.24-0.68) [84].

Further details regarding intraoperative lung-protective ventilation strategies are available elsewhere. (See "Anesthesia for patients with chronic obstructive pulmonary disease", section on 'Mechanical ventilation' and "Mechanical ventilation during anesthesia in adults".)

Arterial blood gases are intermittently sampled (approximately every 60 minutes) if there is a significant gradient between arterial CO₂ tension (PaCO₂) and ETCO₂ due to COPD. This gradient may be exacerbated during aortic cross-clamping due to decreased CO. 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 when surgery is complete [89].

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 a period of postoperative controlled ventilation. (See "Extubation management in the adult intensive care unit".)

EMERGENCY AORTIC SURGERY — Emergency open aortic surgery is generally necessary to manage aortic thrombosis or repair of aortic rupture from any cause. 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 initial evaluation and surgical management of these emergencies can be found in the following topics:

●(See "Management of symptomatic (non-ruptured) and ruptured abdominal aortic aneurysm".)

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

●(See "Management of acute type B aortic dissection".)

●(See "Endovascular methods for aortic control in trauma".)

Evaluation and preoperative management

●A rapid preanesthesia evaluation is performed, similar to that for emergency cardiac surgery. (See "Preoperative evaluation for anesthesia for cardiac surgery", section on 'Emergency surgery'.)

●Two large-bore peripheral intravenous (IV) catheters should be inserted immediately for administration of medications, fluids, and, if necessary, blood transfusions.

●An intra-arterial catheter is inserted as soon as feasible for continuous monitoring of blood pressure (BP). (See 'Monitoring' above.)

●IV 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 if necessary. A relatively low systolic BP (80 to 100 mmHg) is allowed during emergency preoperative imaging studies and transport. Vasopressors and inotropes are administered with caution in the preoperative period to avoid further aortic rupture and exacerbation of bleeding. (See "Surgical and endovascular repair of ruptured abdominal aortic aneurysm", section on 'Preparation'.)

Preparation — Preparation of the following drugs and equipment begins immediately if the patient will require urgent or emergent surgery. Typically, it is necessary to have at least one assistant for these preparations, which may continue even after arrival of the patient in the operating room.

●Monitors – Equipment for insertion and monitoring of the intra-arterial catheter, central venous catheter (CVC), 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/or arrhythmias is likely. (See 'Vasoactive drugs' above.)

●Preparation for transfusion – High-volume transfusion devices 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. 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'.)

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, and 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'.)

Induction and maintenance

●Induction – Severe hypotension may occur during induction of general anesthesia (GA). Thus, before administration of anesthetic induction agents, surgical prepping and draping is completed to facilitate immediate incision and aortic cross-clamp (AXC) application. For a patient with severe hypotension, the AXC is applied as soon as the incision is made. Some surgeons employ an endovascular approach initially, with balloon occlusion of the proximal aorta to restore circulation, as a temporizing measure to allow a controlled anesthetic induction and initiation of an open abdominal procedure to apply the AXC and perform a definitive repair. (See "Surgical and endovascular repair of ruptured abdominal aortic aneurysm", section on 'Criteria for endovascular repair'.)

Rapid sequence induction is typically necessary. We use etomidate or ketamine as the primary induction agent, and we avoid or reduce the doses of adjuvant agents in order 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 IV induction agent. (See "General anesthesia: Intravenous induction agents" and "Rapid sequence induction and intubation (RSII) for anesthesia".)

When patients remain hypertensive at the time of induction (eg, impending or contained aortic rupture in a hypertensive patient), we avoid exacerbation of hypertension 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 – Either an inhalational technique or a total IV anesthesia (TIVA) technique may be used to maintain anesthesia. Typically, low doses of inhalation and IV agents are combined; this strategy may maintain hemodynamic stability by avoiding high doses of any one agent.

Hemodynamic and fluid management — Hemodynamic monitoring and management is similar to that for elective aortic repair, although hemodynamic instability is typically more dramatic when emergency surgery is required due to aortic rupture or thrombosis. (See 'Monitoring' above and 'Hemodynamic management' above.)

Normotensive resuscitation employs fluid and vasopressor resuscitation to maintain target systolic BP >100 mmHg [90]. An alternative strategy has been employed in some centers to target a systolic BP of 50 to 100 mmHg, termed controlled (permissive) hypotension. Although this hypotensive resuscitation strategy has been employed in some management protocols for endovascular repair of ruptured AAA [91,92], there are no randomized trials comparing normotensive resuscitation with a controlled hypotensive resuscitation strategy for emergency open or endovascular aortic repair [90].

Aggressive administration of fluids or RBCs is avoided prior to AXC application due to the risk of dilutional coagulopathy [90,93]. After AXC application, blood products are transfused in a 1:1:1 ratio of RBCs, FFP, and platelets. (See 'Blood salvage and transfusion' above and "Initial management of moderate to severe hemorrhage in the adult trauma patient", section on 'Moderate to severe ongoing hemorrhage'.)

Postoperative management — In the postoperative period, most patients remain intubated and sedated with controlled ventilation after emergency aortic surgery.

POSTOPERATIVE PAIN MANAGEMENT

Thoracic epidural analgesia — We prefer thoracic epidural analgesia (TEA) for postoperative pain management. In a 2016 systematic review of 15 trials that included 1498 patients undergoing open abdominal aortic surgery, addition of epidural analgesia to general anesthesia (GA) provided superior pain relief with reduced pain scores for up to three postoperative days, compared with use of systemic opioid-based analgesia after GA [11]. Other benefits of epidural analgesia included reduced risk of myocardial infarction (risk ratio [RR] 0.54, 95% CI 0.30-0.97), respiratory failure (RR 0.69, 95% CI 0.56-0.85), and gastrointestinal bleeding (odds ratio [OR] 0.20, 95% CI 0.06-0.65), as well as significant mean reductions in time to tracheal extubation (36 hours) and time spent in the intensive care unit (ICU) (six hours). There was no reduction in mortality.

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 [94]. 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 perioperative antithrombotic prophylaxis and intraoperative anticoagulation and reversal. (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 their older age, higher incidence of diabetes and chronic renal disease, longer duration of postoperative epidural analgesic administration, and higher risk of developing infected SEH. Overall, complications of epidural placement are rare and are discussed separately. (See "Adverse effects of neuraxial analgesia and anesthesia for obstetrics".)

The epidural catheter is typically inserted in the immediate preoperative period or in the operating room before induction, and may be used to supplement 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 [29]. 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 [30]. 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 [95].

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'.)

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

Alternative and supplemental techniques for postoperative analgesia — 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 administration of opioid via intravenous (IV) patient-controlled analgesia (PCA). (See "Continuous epidural analgesia for postoperative pain: Technique and management", section on 'Inadequate analgesia'.)

Hypotension or an unacceptable degree of motor block may warrant 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'.)

If neither thoracic nor lumbar epidural analgesia is appropriate due to coagulopathy, anatomical considerations, patient refusal, or emergency surgery, or if attempts to place an epidural catheter are unsuccessful, other methods to control pain are considered. A paravertebral block may be useful in some instances, but would not be placed if coagulopathy is present [96,97] (see "Neuraxial anesthesia/analgesia techniques in the patient receiving anticoagulant or antiplatelet medication"). Intrathecal morphine may be an option in some patients [98]. The most common alternative technique is administration of IV systemic opioids via PCA, typically employed as part of a multimodal strategy that includes nonopioid analgesic agents or regional techniques [99-101]. For example, a transverse abdominis plane (TAP) block may be performed to provide partial relief [102]. (See "Use of opioids for postoperative pain control" and "Thoracic paravertebral block procedure guide" and "Transversus abdominis plane (TAP) blocks procedure guide".)

Management of acute perioperative pain is discussed in detail separately. (See "Approach to the management of acute pain in adults".)

After emergency open aortic surgery, we employ a pain control regimen suitable for critically ill patients. (See "Pain control in the critically ill adult patient".)

COMPLICATIONS — Complications of open aortic surgery are discussed separately:

●(See "Management of symptomatic (non-ruptured) and ruptured abdominal aortic aneurysm", section on 'Morbidity and mortality'.)

●(See "Surgical and endovascular repair of ruptured abdominal aortic aneurysm", section on 'Complications'.)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world 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 assessment of cardiovascular, pulmonary, and renal risks, as well as 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 central venous catheter (CVC) is often inserted to provide large-bore venous access for fluid and blood administration and for vasoactive drug infusions. (See 'Standard monitoring' 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 aortic pathology. (See 'Transesophageal echocardiography' above.)

●Induction and maintenance of general anesthesia – We prefer a volatile inhalation anesthetic (eg, sevoflurane, isoflurane, or desflurane) as the primary agent to maintain GA, although total intravenous (IV) anesthesia (TIVA) is an acceptable alternative. Nitrous oxide (N₂O) is avoided because of bowel distension and postoperative nausea and vomiting (PONV). (See 'General anesthesia' above.)

●Fluid management – We suggest goal-directed crystalloid fluid therapy to maintain normovolemia using dynamic parameters to assess fluid responsiveness (figure 1), rather than static parameters such as urine output (UO) or central venous pressure (Grade 2C). We prefer transesophageal echocardiography (TEE) to assess dynamic changes in left ventricular (LV) cavity size; respirophasic variation in the intra-arterial pressure waveform is also used to guide fluid therapy (movie 1). (See 'Goal-directed fluid therapy' above.)

●Blood management – We suggest blood salvage rather than relying on transfusion of allogeneic blood (Grade 2B). We transfuse salvaged or crossmatched red blood cells (RBCs) if hemoglobin is ≤8 g/dL, or ≤9 g/dL if there is evidence of ongoing bleeding or cardiac or other organ ischemia. (See 'Blood salvage and transfusion' above and "Surgical blood conservation: Intraoperative blood salvage".)

●Hemodynamic management – Hemodynamic changes often require specific management during aortic cross-clamping (figure 4 and figure 5) and upon unclamping (figure 6). Vasopressors and inotropic agents, as well as vasodilators are prepared in advance and immediately available (table 7 and table 8). (See 'Management of aortic cross-clamping' above and 'Management of aortic unclamping' above and 'Vasoactive drugs' above.)

●Temperature management – We employ devices for warming the upper and lower body and all IV fluids and blood in order to maintain normothermia (temperature ≥35.5°C). (See 'Temperature management' above.)

●Ventilation management – We recommend lung-protective ventilation with low tidal volumes of 6 to 8 mL/kg (Grade 1B). (See 'Ventilation management' above.)

●Postoperative pain management – For management of postoperative pain, we recommend continuous thoracic epidural analgesia (TEA) (Grade 1B). The use of TEA provides superior pain relief and reduces other complication rates compared with use of systemic opioid-based analgesia after general anesthesia (GA). A thoracic epidural is typically inserted prior to anesthetic induction and may be used as part of an anesthetic technique that combines epidural and GA. The timing of epidural placement and removal is carefully coordinated with planned administration of intraoperative heparin, as well as perioperative administration of antithrombotic prophylactic medications, in order to minimize the risk of spinal epidural hematoma. Combinations of local anesthetic plus an opioid achieve a balance between analgesic efficacy and adverse side effects of each agent. (See 'Planning for postoperative pain management' above and 'Epidural anesthesia' above and 'Thoracic epidural analgesia' above.)

●Emergency aortic surgery – Some aspects of anesthetic management are modified for emergency aortic surgery. Aggressive administration of fluids or RBCs is avoided until after aortic cross-clamp (AXC) application; then, blood products are transfused in a 1:1:1 ratio of RBCs, fresh frozen plasma (FFP), and platelets. (See 'Emergency aortic surgery' above.)