Anesthesia for open descending thoracic aortic surgery

INTRODUCTION — Open surgical repair of the descending thoracic aorta is used in selected patients to manage thoracic aortic pathology such as aneurysm, dissection, or injury. Although an endovascular surgical approach (ie, thoracic endovascular aortic repair [TEVAR]) is often preferred due to a lower incidence of perioperative complications, open repair or a hybrid open/endovascular procedure is necessary in some cases. Despite advances in surgical, perfusion, and anesthetic techniques, mortality and significant morbidity may occur during open repair.

This topic will review anesthetic management for patients undergoing open surgical repair of the descending thoracic aorta. Anesthetic considerations for patients with cardiovascular disease are similar across etiologies. Surgical considerations for open repair of the thoracic aorta are reviewed in a separate topic. (See "Overview of open surgical repair of the thoracic aorta", section on 'Descending aorta'.)

PREANESTHETIC ASSESSMENT

Risk assessment — Perioperative morbidity and mortality after thoracic aortic surgery is high compared with most elective surgical procedures due to potential for large blood loss, prolonged duration of surgery, and ischemic or embolic complications affecting the spinal cord, lower extremities, or vital organs [1].

Paraparesis/paraplegia — The risk of spinal cord ischemia (SCI) following open thoracic aortic surgery resulting in paraparesis or paraplegia has been reduced to 1 to 6 percent by improvements in surgical and anesthetic techniques, (comparable to the 4 to 7 percent risk reported for endovascular repair) [1-5]. More extensive aortic surgical procedures are associated with the highest risk. Overall, the location, extent, and effect of thoracic aortic pathology on spinal cord vascular supply determine the risk of spinal cord ischemia [6-8]. One study has noted that the incidence of SCI is higher for repair of a thoracoabdominal aneurysm (7.6 percent) (figure 1) compared with a descending thoracic aortic aneurysm (3.5 percent) (figure 2) [9]. (See "Spinal cord infarction: Epidemiology and etiologies", section on 'Vascular anatomy'.)

Strategies for spinal cord protection during thoracic aortic surgery are reviewed below and in a separate topic. (See 'Review of the surgical plan' below and "Overview of open surgical repair of the thoracic aorta", section on 'Descending aorta'.)

Atherosclerosis complications — Patients with aortic atherosclerotic disease have a high perioperative risk for cardiac complications including myocardial infarction or death because most have generalized atherosclerotic and coronary arterial disease (table 1 and table 2) [1,10,11]. General principles for anesthetic management of patients with ischemic heart disease are reviewed separately. (See "Anesthesia for noncardiac surgery in patients with ischemic heart disease".)

Patients undergoing open thoracic aortic surgery also have a high risk of stroke due to the likelihood of pre-existing cerebrovascular disease as well as the potential for embolism of aortic atherosclerotic debris into the cerebral circulation during surgical manipulation of the aortic arch [1,12-14]. Since ischemic or embolic cerebral injury is exacerbated by hypotension, a higher proximal mean arterial pressure (MAP) of 80 to 100 mmHg is typically targeted during descending thoracic aortic surgery, as noted below (see 'Control of aortic blood pressure' below). This may be particularly important in patients with longstanding hypertension that may have caused a shift in the cerebral autoregulation threshold [15]. (See "Anesthesia for patients with hypertension".)

Renal dysfunction — Renal dysfunction is associated with adverse outcomes after surgery [16-19]. Elevated preoperative serum creatinine is a predictor of postoperative renal dysfunction after either abdominal or thoracic aortic surgery (table 1) [16,20,21]. Prolonged aortic cross-clamping, embolism of atherosclerotic debris into the renal arteries, hemodynamic instability, blood loss, or dehydration may exacerbate or cause new renal dysfunction.

Routine strategies to preserve renal function during vascular surgery include ensuring adequate preoperative hydration, then optimizing intravascular volume status throughout the perioperative period. (See 'Strategies to prevent renal and visceral ischemia' below.)

Review of the surgical plan — Surgical strategies to prevent spinal cord ischemia and injury during descending thoracic aortic surgery are discussed separately. (See "Overview of open surgical repair of the thoracic aorta", section on 'Preoperative evaluation and preparation'.)

Preoperative review of the surgical approach is necessary to plan anesthetic care. Examples include [2,22]:

●Use of partial left heart bypass – Partial left heart bypass is often selected by the surgeon to maintain distal aortic perfusion, thereby maintaining spinal cord perfusion during the period of aortic cross-clamping, particularly if a long cross-clamp time is anticipated [22]. (See "Overview of open surgical repair of the thoracic aorta", section on 'Descending aorta'.)

Anesthetic implications for planned use of partial left heart bypass for distal aortic perfusion include:

•Two sites are selected for intra-arterial monitoring, an upper body site (eg, the right radial artery) and a lower body site (eg, a femoral artery). (See 'Cardiovascular monitors' below.)

•MAP is routinely maintained ≥80 mmHg in the upper body (measured in the right radial intra-arterial catheter) and ≥50 mmHg in the lower body (measured in the femoral intra-arterial catheter). (See 'Control of aortic blood pressure' below.)

●Use of systemic hypothermia – Permissive hypothermia (approximately 34°C) is typically allowed prior to aortic cross-clamping [22]. In some cases, mild hypothermia (approximately 32°C) is induced with the aid of a heat exchanger incorporated in the partial left heart bypass perfusion circuit [3,22]. Anesthetic implications of hypothermia include:

•Planned use of systemic hypothermia guides selection of temperature monitoring sites and warming devices. (See 'Temperature monitors' below.)

•During hypothermia, responses to both motor evoked potentials (MEPs) and somatosensory evoked potentials (SSEPs) may be masked or eliminated. (See "Neuromonitoring in surgery and anesthesia", section on 'Temperature'.)

•Rewarming after a hypothermic period must be accomplished gradually, with care to avoid systemic hyperthermia. The anesthesia team warms all intravenous fluids and uses a forced-air warming blanket. The surgical team irrigates the thorax or abdomen with warmed saline. Some centers use a heat exchanger in the partial left heart bypass perfusion circuit to accomplish rewarming [3].

•Adverse perioperative effects associated with induced hypothermia increase risk of coagulopathy. Other potential adverse effects include cardiac arrhythmias, hyperglycemia, and decreased metabolism of anesthetic agents and other drugs (table 3). (See "Perioperative temperature management", section on 'Consequences'.)

●Placement of an intrathecal catheter – The decision to insert an intrathecal catheter is based on indications for monitoring cerebrospinal fluid (CSF) pressure with drainage of CSF to improve spinal cord perfusion pressure (SCPP) if spinal cord ischemia becomes evident during neuromonitoring. (See 'Cerebrospinal fluid (CSF) pressure monitoring' below and 'Maintenance of low CSF pressure with CSF drainage' below and 'Neuromonitoring for spinal cord ischemia' below.)

●Strategies to maintain spinal cord circulation – In addition to maintaining collateral circulation to the spinal cord by controlling MAP (see 'Control of aortic blood pressure' below), the surgeon may employ selective perfusion or reimplantation of segmental intercostal and lumbar arteries, or selective perfusion of renal and visceral arteries. (See "Overview of open surgical repair of the thoracic aorta", section on 'Descending aorta'.)

Review of preoperative tests

●Typing and cross-matching – We perform typing and cross-matching of six units of red blood cells (RBCs), six units of fresh frozen plasma, and one unit of platelets due to the potential for large blood loss and ensure that these blood products are available prior to surgical incision.

●Electrocardiogram – A preoperative electrocardiogram (ECG) is obtained in patients with known significant cardiovascular disease to serve as a baseline if the postoperative ECG is abnormal. Additional cardiac testing is indicated only in patients with changes in cardiac symptoms or functional status. (See "Evaluation of cardiac risk prior to noncardiac surgery".)

●Laboratory tests – Preoperative laboratory tests (complete blood count, tests of hemostasis, electrolytes, glucose, blood urea nitrogen [BUN], creatinine) are typically available. These provide baseline values for comparison with intraoperative point-of-care (POC) and postoperative test results.

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 any chronically administered anticoagulant or antiplatelet medications is timed to allow safe placement of an intrathecal catheter. The optimal timing of neuraxial catheter placement varies for different medications, as detailed in a separate topic. (See "Neuraxial anesthesia/analgesia techniques in the patient receiving anticoagulant or antiplatelet medication".)

MONITORING

Standard monitors — In addition to standard monitors (table 4), a bladder catheter with a temperature probe is inserted after induction to measure urine output and as an additional temperature monitor. (See 'Temperature monitors' below.)

Temperature monitors — An oropharyngeal temperature probe to estimate upper body temperature, and a bladder catheter temperature probe to estimate lower body and core temperatures are both continuously monitored whether or not partial left heart bypass is used. Temperature monitoring is particularly important during and after a period of deliberate systemic hypothermia with gradual rewarming and maintenance of normothermia during the remainder of the procedure.

Cardiovascular monitors

●Proximal and distal intra-arterial catheters – We insert two intra-arterial catheters for continuous monitoring of arterial blood pressure (BP); one is inserted in the right radial artery to monitor BP proximal to the thoracic aortic surgical site. This is typically accomplished before induction to detect and optimally treat hypotension or hypertension that may occur during administration of anesthetic induction agents, laryngoscopy, and endotracheal intubation. Also, an intra-arterial catheter is inserted in a femoral artery (typically after induction) to monitor BP distal to the thoracic aortic surgical site. Since patients with thoracic aortic aneurysm often have peripheral arterial atherosclerosis, discrepancies in BP between upper versus lower extremities and right versus left upper extremities may be noted. Any differences should be communicated to the operating surgeon.

Intra-arterial catheters are also used to evaluate respirophasic variations in the arterial pressure waveform (figure 3) (see "Intraoperative fluid management", section on 'Dynamic parameters to assess volume responsiveness'), and to intermittently obtain blood samples for laboratory tests. (See 'Point-of-care laboratory testing' below.)

●Central venous catheter and intravascular access – We insert an introducer sheath or large-bore central venous catheter (CVC) in an internal jugular vein to provide venous access for fluid and blood administration and for infusion of vasoactive drugs. Although central venous pressure (CVP) is typically measured to provide supplemental data regarding intravascular volume status, it is a poor predictor of fluid responsiveness [23-27]. (See "Intraoperative fluid management", section on 'Traditional static parameters'.)

Since estimated blood loss often exceeds 1500 mL, either a rapid infusion catheter or two large bore peripheral intravascular (IV) catheters may be inserted to provide additional IV access.

●Pulmonary artery catheter – If the patient has a history of symptomatic heart failure or pulmonary hypertension, a pulmonary artery catheter (PAC) is typically also inserted.

●Transesophageal echocardiography – Similar to patients undergoing open abdominal aortic surgery, we employ transesophageal echocardiography (TEE) during open thoracic aortic surgery. Episodes of severe hemodynamic instability are detected and treated, particularly during aortic cross-clamping and unclamping. (See "Anesthesia for open abdominal aortic surgery", section on 'Hemodynamic management'.)

Continuous TEE monitoring is used to monitor IV volume status to avoid hypovolemia or hypervolemia, and to monitor cardiac function and detect regional and global ventricular dysfunction (figure 4 and figure 5), as discussed separately. (See "Intraoperative transesophageal echocardiography for noncardiac surgery", section on 'Volume status' and "Intraoperative transesophageal echocardiography for noncardiac surgery", section on 'Ventricular function'.)

TEE is also used to detect aortic pathology such as atheromas, thromboembolism, air embolism, or aortic dissection resulting from cannulation or cross clamping the aorta. Even if TEE is not used electively, rapid deployment may be urgently needed to diagnose causes of hemodynamic instability or cardiovascular collapse (ie, "rescue" TEE). (See "Intraoperative rescue transesophageal echocardiography (TEE)".)

Neuromonitoring for spinal cord ischemia — Neuromonitoring with motor evoked potentials (MEPs) and somatosensory evoked potentials (SSEPs) provides continuous assessment of spinal cord function during aortic surgery, with the goal of detecting evidence of spinal cord ischemia so that interventions can be immediately initiated to avoid irreversible injury [2,22,28]. (See "Neuromonitoring in surgery and anesthesia", section on 'Motor evoked potentials' and "Neuromonitoring in surgery and anesthesia", section on 'Somatosensory evoked potentials'.)

If changes indicating spinal cord ischemia are noted during neuromonitoring of MEPs and/or SSEPs, typically after cross-clamping of the thoracic aorta, the anesthesiologist, surgeon, and neuromonitoring team should urgently work together to confirm the changes, determine the etiology, and initiate interventions to treat the ischemia (algorithm 1). (See "Neuromonitoring in surgery and anesthesia", section on 'Managing electrophysiologic changes' and 'Intraoperative management' below.)

Motor evoked potentials (MEPs) — Transcranial stimulation of MEPs involves electrical stimulation of the scalp overlying the motor cortex, which generates waves that travel down the corticospinal tract to the nerve root and the peripheral nerve, which results in muscle action potentials in a peripheral muscle group (eg, the anterior tibialis), where the evoked response is recorded (figure 6). During open aortic surgery, transesophageal stimulation of MEPs may be a feasible alternative to transcranial stimulation [29]. (See "Neuromonitoring in surgery and anesthesia", section on 'Motor evoked potentials'.)

MEP monitoring has implications for anesthetic management including avoidance of neuromuscular blocking and use of a total intravenous anesthesia (TIVA) technique with only a low dose of a volatile inhalation agent during the period that MEPs are being monitored (table 5) [30-32]. Nitrous oxide (N₂O) is also avoided due to its similar effects on MEPs. Details are discussed separately. (See "Neuromonitoring in surgery and anesthesia", section on 'MEP monitoring'.)

Limitations of MEP monitoring for spinal cord ischemia include the following caveats:

●Reversible intraoperative changes do not correlate with paraplegia [33,34].

●Intraoperative MEP monitoring has a low sensitivity but high specificity (37.8 and 95.5 percent, respectively) for predicting motor deficits at the time of hospital discharge [34,35]. However, MEPs <25 percent of control values are not necessarily associated with severity of spinal cord damage [35].

●If hypothermia below 32°C is employed, latencies and stimulation thresholds are increased (although MEP waveforms can often be detected to core temperatures as low as 31 to 34°C) [36-38]. (See "Neuromonitoring in surgery and anesthesia", section on 'Temperature'.)

●Interpretation of MEPs may be challenging since intraoperative changes that may indicate ischemia are not standardized [33].

Somatosensory evoked potentials (SSEPs) — Monitoring of SSEPs involves electrical stimulation of distal nerves of the lower extremity (eg, the posterior tibial and peroneal nerves), then recording the resultant cortical electrical potentials via scalp electrodes to monitor continuity of lateral and posterior column function (figure 7). SSEP monitoring has implications for anesthetic management similar to those for monitoring of MEPs (table 5) [30-32]. Details are discussed separately. (See "Neuromonitoring in surgery and anesthesia", section on 'Somatosensory evoked potentials'.)

Limitations of SSEP monitoring for monitoring spinal cord ischemia include:

●The posterior columns monitored with SSEPs control only sensory function, while the anterior (unmonitored) columns controlling motor function are of greater interest during cross-clamping of the descending thoracic aorta.

●Although absence of changes in SSEPs provides valuable information and the negative predictive value is >99 percent, the positive predictive value of SSEPs may be as low as 60 percent [3].

●Hypothermia can delay conduction time and decrease amplitude, creating a false positive response that appears similar to ischemic SSEP changes [37,38]. (See "Neuromonitoring in surgery and anesthesia", section on 'Temperature'.)

Cerebrospinal fluid (CSF) pressure monitoring — CSF pressure is monitored in patients at high risk for paraparesis/paraplegia due to previous aortic surgery, stenting, or extended aortic segment coverage (figure 8). Drainage of CSF to lower CSF pressure can improve spinal cord perfusion pressure if evidence of spinal cord ischemia develops (algorithm 1) [2,22,39-44]. Candidates for CSF pressure monitoring and drainage include those with known preoperative and/or likely intraoperative risk factors for spinal cord ischemia [39-44]. (See 'Maintenance of low CSF pressure with CSF drainage' below and "Overview of open surgical repair of the thoracic aorta", section on 'Anesthesia, monitoring, and organ protection'.)

The technique involves insertion of a lumbar intrathecal catheter into the subarachnoid space at the L3-L4 level. The intrathecal catheter is typically placed by the anesthesiologist on the day of surgery immediately before induction of general anesthesia. However, in some centers, the catheter is inserted the day before surgery, either by an anesthesiologist, or by a neuroradiologist with the aid of fluoroscopic guidance, particularly if there is anticipated difficulty of a failed attempt with drain insertion [45]. The potential benefit of catheter insertion on the day before surgery is prevention of case cancellation if attempted placement is traumatic (bloody); the disadvantage is an extra day of hospitalization with its associated costs.

In a systematic review of 4714 patients including open repair of thoracic or thoracoabdominal aortic pathology (34 studies), risks associated with intrathecal catheter placement for CSF drainage included [46]:

●Severe complications such as epidural hematoma, intracranial hemorrhage, subarachnoid hemorrhage, meningitis, or catheter drainage-related neurologic deficits occurred in 2.5 percent.

●Moderate complications such as spinal headache, CSF leak requiring intervention, or catheter fracture requiring surgical or nonsurgical removal occurred in 3.7 percent.

●Minor complications such as puncture-site bleeding, bloody spinal fluid, CSF leak not requiring intervention, hypotension, or occluded or dislodged catheters occurred in 2 percent. Mortality related to CSF drainage was reported to be 0.9 percent.

CSF drainage is a strategy to increase spinal cord perfusion to prevent and/or treat spinal cord ischemia. (See 'Maintenance of low CSF pressure with CSF drainage' below.)

Cerebral oximetry to monitor for cerebral ischemia — Cerebral oximetry monitoring with near-infrared spectroscopy monitoring has been used to detect unilateral or bilateral cerebral hypoperfusion. Unilateral cerebral desaturation may indicate local disruption in cerebral blood flow (eg, new arterial dissection); detection allows immediate notification of the surgeon [47].

If bilateral (presumably global) decrease in cerebral oxygen saturation >10 percent compared with baseline becomes evident, efforts to increase oxygen delivery may include [14]:

●Increasing mean arterial pressure (MAP) by administering a vasopressor

●Ensuring adequate cardiac output

●Ensuring adequate oxygen saturation of systemic arterial blood, and increasing the fraction of inspired oxygen (FiO₂) if necessary

●Ensuring that arterial partial pressure of carbon dioxide (PaCO₂) is not <35 mmHg

●Decreasing cerebral metabolic rate of oxygen consumption (CMRO₂) by deepening anesthesia

●Increasing blood oxygen-carrying capacity with red blood cell (RBC) transfusion if Hgb is <8 g/dL

Point-of-care laboratory testing — Point-of-care (POC) testing during open aortic surgery includes arterial blood gases, pH, and lactate levels, hemoglobin, electrolytes, and glucose. Activated clotting time (ACT) is measured when anticoagulation with heparin is used. Standard and POC testing of hemostasis (eg, thromboelastography [TEG] or rotational thromboelastometry [ROTEM]) are used if there are clinical signs of coagulopathy or significant bleeding. (See "Intraoperative transfusion and administration of clotting factors", section on 'Intraoperative diagnostic testing'.)

INTRAOPERATIVE MANAGEMENT

Anesthetic techniques

Induction and airway management — Most patients undergoing aortic surgery are at risk for ischemic heart disease. Thus, techniques to induce general anesthesia should minimize risk of myocardial ischemia, with avoidance of hypotension, hypertension, and tachycardia, as discussed separately. (See "Anesthesia for noncardiac surgery in patients with ischemic heart disease", section on 'Induction'.)

Since cross-clamping above the diaphragm is necessary, a double lumen endotracheal tube (DLT) or bronchial blocker is inserted to achieve one lung ventilation. These techniques are discussed in separate topics. (See "One lung ventilation: General principles" and "Lung isolation techniques".)

Positioning — Positioning for a left-sided posterolateral thoracotomy is in the right semi-lateral decubitus position. The table is flexed at the patient's waist. Details regarding safe positioning are discussed separately. (See "Patient positioning for surgery and anesthesia in adults", section on 'Lateral decubitus'.)

Maintenance — If neuromonitoring is planned, maintenance of anesthesia is achieved with a balanced anesthetic technique (eg, a volatile inhalation agent administered at ≤0.5 MAC (table 6), plus infusions of dexmedetomidine and an opioid) or total intravenous anesthesia (TIVA). Other centers use infusions of propofol plus an opioid (eg, fentanyl, sufentanil, remifentanil), with or without a ketamine infusion as an adjuvant agent to augment motor evoked potential (MEP) and somatosensory evoked potential (SSEP) amplitude [48]. These regimens allow elicitation of both MEP and SSEP responses in most patients (table 5). (See "Neuromonitoring in surgery and anesthesia", section on 'Anesthetic effects on neuromonitoring'.)

If neuromonitoring is not planned, an inhalation anesthetic technique is often selected because of the advantage of rapid titration based on the patient's current hemodynamics [10,11]. Also, inhalation agents have likely cardioprotective effects, although this has not been demonstrated in aortic surgery. A TIVA technique with propofol is a reasonable alternative [49-52]. (See "Anesthesia for noncardiac surgery in patients with ischemic heart disease", section on 'Maintenance'.)

Antibiotic prophylaxis — In addition to initial antibiotic prophylaxis, antibiotics require redosing during the procedure since the duration of surgery is often prolonged. Details are discussed in a separate topic. (See "Antimicrobial prophylaxis for prevention of surgical site infection in adults", section on 'Vascular surgery'.)

Hemodynamic management

Control of aortic blood pressure — Maintenance of adequate mean arterial pressure (MAP) to maintain collateral circulation during thoracic aortic surgery is particularly critical in patients with high risk for paraparesis/paraplegia. MAP is incrementally increased if evidence of spinal cord ischemia develops (algorithm 1) [39-44].

Proximal aortic blood pressure control by the anesthesiologist aims to keep MAP ≥80 mmHg using vasopressors or fluid administration, to maintain adequate spinal cord perfusion and prevent or treat spinal cord ischemia noted with neuromonitoring [2,3,15,22]. If central venous pressure (CVP) is higher than cerebrospinal fluid (CSF) pressure, preferentially use vasopressor therapy, rather than volume expansion (see 'Maintenance of low CSF pressure with CSF drainage' below). The goal for proximal aortic MAP is ≥80 mmHg, whether the surgeon uses partial left heart bypass or simply cross-clamps the thoracic aorta without the use of partial bypass (ie, "clamp and sew" technique). Patients with longstanding pre-existing hypertension have a particularly high risk for developing spinal cord ischemia with resultant paraparesis/paraplegia and may need further augmentation of MAP to restore spinal cord perfusion [53]. Thus, MAP is rapidly increased in 5 mmHg increments to >90 mmHg, or as high as 110 mmHg in some patients with persistent evidence of spinal cord ischemia.

Cross-clamping of the thoracic aorta typically results in a pronounced increase in MAP proximal to the aortic clamp, as well as increases in production of CSF, CSF pressure, and intracranial pressure (ICP). Thus, spinal cord ischemia is most effectively prevented and/or treated by maintaining proximal MAP ≥80 mmHg (or near the patient's preoperative baseline if that value is somewhat higher), while simultaneously decreasing CSF pressure by draining CSF to maintain CSF pressure at 8 to 10 mmHg. (See 'Maintenance of low CSF pressure with CSF drainage' below.)

These goals will ensure that spinal cord perfusion pressure (SCPP) is ≥70 mmHg according to the following formula:

The rationale for maintaining a relatively high SCPP is to ensure flow through the collateral network of small vessels within the spinal canal, which communicates with the major anterior and posterior spinal arteries and with vessels in perivertebral tissue, paraspinal muscles, and hypogastric vessels [7]. Physiologic reserves for perfusion exist via the spinal cord collateral networks, and this collateral blood flow may be the main determinant of spinal cord perfusion [2,22]. During a period of thoracic aortic cross-clamping, perfusion of the spinal cord is variable and tenuously dependent upon this collateral circulation via control of the proximal aortic blood pressure [7]. Retrospective studies in patients undergoing open repair of a descending thoracic or thoracoabdominal aneurysm have noted that perioperative hypotension below 70 mmHg is an independent predictor of postoperative neurologic deficit [15,42,54,55].

In addition to adequate blood flow, optimal oxygen delivery to the spinal cord is necessary to prevent spinal cord ischemia. This is achieved by maintaining cardiac output and optimal systemic O₂ content, including normal to high hemoglobin (Hgb) saturation (measured with pulse oximetry) and/or arterial partial pressure of oxygen (PaO₂) (measured with arterial blood gases), as well as adequate Hgb levels (≥8 g/dL) [56].

Management of aortic cross-clamping and unclamping

●Aortic cross-clamping – Aortic cross-clamping causes a sudden, large increase in left ventricular (LV) systolic afterload that can lead to myocardial ischemia and/or LV failure (figure 9) [57-64]. The level of clamping is a factor; higher-level thoracic, or suprarenal compared with infrarenal clamping causes more marked hemodynamic instability. Management is described separately. (See "Anesthesia for open abdominal aortic surgery", section on 'Management of aortic cross-clamping'.)

Regional wall motion abnormalities (RWMAs) indicating ischemia may progressively worsen after aortic clamping and may progress to global severe hypokinesis if the sudden elevation in cardiac preload is not ameliorated with partial left heart bypass (movie 1). Early recognition of myocardial ischemia or ventricular dysfunction facilitates management [58]. (See "Intraoperative transesophageal echocardiography for noncardiac surgery", section on 'Regional LV systolic function'.)

●Aortic unclamping – Removal of the aortic cross-clamp results in a sudden decrease in systemic vascular resistance (SVR) and hypotension (figure 10) [64]. This is due to the reperfusion syndrome, with hypoxia-mediated reactive hyperemia and metabolic (lactic) acidosis [64,65]. Preload is decreased due to venodilation, and myocardial contractility is decreased due to acidosis. Hypotension may be profound, particularly with unclamping from a higher (eg, thoracic, suprarenal) level [57]. Also, metabolic acidosis and washout of ischemic muscle tissue may result in hyperkalemia, malignant arrhythmias, and cardiac arrest. Management is described separately. (See "Anesthesia for open abdominal aortic surgery", section on 'Management of aortic unclamping'.)

Maintenance of low CSF pressure with CSF drainage — Intrathecal CSF pressure monitoring with CSF drainage is frequently used to maintain low CSF pressure (ie, 10 mmHg) to achieve optimal spinal cord protection [2,3,22,39-44,66,67]. (See 'Cerebrospinal fluid (CSF) pressure monitoring' above and "Overview of open surgical repair of the thoracic aorta", section on 'Anesthesia, monitoring, and organ protection'.)

Guidelines for intrathecal catheter management, CSF pressure monitoring, and CSF drainage include the following:

●Initial management:

•Record opening pressure and zero the CSF pressure transducer at the right atrial level.

•Monitor CSF pressure continuously.

•If CSF pressure is >12 mmHg, drain CSF in increments until pressure is 10 mmHg.

●Intraoperative factors that warrant timely CSF drainage in increments until pressure is ≤10 mmHg in order to increase SCPP include [2,42-44,68]:

•Signs of spinal cord ischemia noted with neuromonitoring of MEPs and/or SSEPs (ie, decreased signal amplitude). Also, augment MAP as necessary (algorithm 1). (See 'Neuromonitoring for spinal cord ischemia' above and 'Control of aortic blood pressure' above.)

•CSF pressure >12

•Significant backbleeding from segmental arteries (noted in the surgical field)

•Injury to an internal iliac artery

●During all perioperative periods:

•Limit CSF drainage to <20 mL during the first hour of surgery.

•Limit CSF drainage to <40 mL during any four-hour period.

•If CSF becomes bloody, discontinue drainage immediately and obtain magnetic resonance imaging (MRI) of the spinal cord as soon as feasible.

The rationale for CSF drainage involves decreasing pressure in the subarachnoid space to reduce resistance to blood flow through the collateral network of small vessels within the spinal canal, thereby improving perfusion to the spinal cord [2,7]. As noted above, an optimal strategy involves both CSF drainage to maintain CSF pressure at ≤10 mmHg, as well as maintenance of MAP ≥80 mmHg, thereby ensuring a SCPP ≥70 mmHg [2,44]. (See 'Control of aortic blood pressure' above.)

In a 2016 meta-analysis, CSF drainage was effective for preventing neurologic injury (10 studies; 2103 patients), reducing the risk of SCI following thoracoabdominal aortic aneurysm (TAAA) repair by nearly one-half (odds ratio [OR] 0.42, 95% CI 0.25-0.7) [69]. Although CSF drainage is effective for preventing SCI, it has been associated with other complications. A 2018 meta-analysis that included 34 studies with 4714 patients undergoing open and endovascular descending thoracic aneurysm (DTA) or TAAA repair reported 6.5 percent rate of CSF drainage-related complications [46]. Complications were minor in 2 percent, moderate requiring intervention in 3.7 percent, and severe in 2.5 percent including epidural hematoma, intracranial or subarachnoid hemorrhage, and/or catheter related neurologic deficit. As noted above, CSF drainage is typically used in conjunction with control of proximal MAP, as well as with neuromonitoring to assess the effects of these interventions [2,68]. (See 'Control of aortic blood pressure' above and 'Neuromonitoring for spinal cord ischemia' above.)

Strategies to prevent renal and visceral ischemia — Fastidious control of proximal MAP aids in maintaining perfusion to the kidneys and viscera (see 'Control of aortic blood pressure' above). Other routine strategies to preserve renal function during vascular surgery include maintaining optimal intravascular volume status and hemodynamic stability throughout the perioperative period.

We do not administer furosemide, mannitol, or dopamine to provide renal protection, similar to management of patients undergoing open abdominal aortic surgery.

Management of anticoagulation, bleeding, and hemostasis — Prior to cross-clamping the aorta, unfractionated heparin is administered to achieve systemic anticoagulation. When partial left heart bypass is used, our standard protocol includes dosing heparin with an activated clotting time (ACT) target of approximately 250 seconds. After completion of the repair, the effects of heparin are reversed with protamine to achieve hemostasis. (See "Protamine: Administration and management of adverse reactions during cardiovascular procedures".)

In many centers, prophylactic antifibrinolytic therapy (epsilon-aminocaproic acid [EACA] or tranexamic acid [TXA]) is often administered to decrease the risk of perioperative bleeding [1,70-72]. A 2023 meta-analysis identified two trials comparing systemic administration of TXA with placebo in participants undergoing vascular surgery [72]. The larger of these, the POISE-3 trial, included vascular and other types of high-risk surgical procedures. Significantly reduced overall bleeding (composite of life-threatening, major and critical organ bleeding) was noted in the TXA group (hazard ratio [HR] 0.76, 95% CI 0.67-0.87). However, the difference was not significant within the vascular surgery subgroup (HR 0.86, 95% CI 0.64-1.13) [72]. The reviewers noted limited data and uncertainty regarding whether TXA administration improved clinically important outcomes (ie, mortality, need for reoperation due to bleeding, number of patients requiring allogeneic blood transfusion, number of red blood cells [RBCs] transfused per patient) [72]. (See "Intraoperative use of antifibrinolytic agents".)

Blood salvage is used since significant blood loss (eg, >1500 mL) and transfusion of allogeneic RBCs is likely (see "Surgical blood conservation: Intraoperative blood salvage"). Autologous salvaged or allogeneic RBCs are transfused as necessary to maintain the Hgb level ≥8 g/dL. We employ point-of-care (POC) viscoelastic tests of hemostasis (eg, thromboelastography [TEG] or rotational thromboelastometry [ROTEM]) to guide decision-making regarding transfusion of fresh frozen plasma or platelets. Fibrinogen concentrate may be used to treat hypofibrinogenemia (ie, fibrinogen concentration <100 mg/dL) [73,74]. (See "Intraoperative transfusion and administration of clotting factors", section on 'Indications and risks for specific blood components'.)

Residual hypothermia (either permissive or induced) that was used to prevent or minimize spinal cord ischemia increases risk of perioperative coagulopathy. (See "Perioperative temperature management", section on 'Consequences'.)

EARLY POSTOPERATIVE MANAGEMENT

●Postoperative controlled ventilation – In most patients, extubation may not be feasible at the end of the surgical procedure due to residual hypothermia (temperature <35.5°C), hemodynamic instability, coagulopathy, failure to meet standard extubation criteria, or uncorrected hypoxemia, hypercarbia, or acidosis. Sedation and controlled ventilation are typically necessary for several hours after surgery. Patients are transported to an intensive care unit (ICU) for further monitoring and care. (See "Transport of surgical patients".)

●Management of delayed paraparesis – Urgent management of delayed paraparesis or paraplegia is discussed in a separate topic (algorithm 2).

●Management of postoperative pain – Patients undergoing open thoracic aortic surgical repair have large thoracic or thoracoabdominal incisions causing significant postoperative pain. Ideally, postoperative pain is managed with multimodal strategies. These may include (see "Postoperative care after cardiac surgery", section on 'Analgesia'):

•Regional anesthesia with a local anesthetic administered via bilateral thoracic paravertebral blocks (PVBs) is useful to provide safe and effective supplemental analgesia, and may decrease the incidence of postoperative reintubation and pneumonia, as well as improve hemodynamic stability after open thoracic aortic repair [75-79]. Although many clinicians are not familiar with the PVB technique, direct surgical placement into the open chest is an option in open thoracotomy cases. (See "Anesthesia for open pulmonary resection", section on 'Paravertebral block'.)

Similar to other procedures requiring thoracotomy, other regional analgesic techniques for thoracotomy incisions include the serratus anterior plane (image 1), erector spinae plane (figure 11), pectoral nerve (image 1), or intercostal nerve blocks (figure 12 and figure 13 and image 2) [80-83]. Block duration may be prolonged by a continuous catheter technique [83]. (See "Thoracic nerve block techniques", section on 'Fascial plane blocks of the chest wall'.)

However, for practical reasons related to maintenance of spinal cord perfusion pressure, placement of a thoracic epidural catheter is avoided. (See "Postoperative care after cardiac surgery", section on 'Neuraxial and regional anesthetic techniques'.)

•Intravenous patient-controlled analgesia (PCA) with an opioid is usually necessary to provide both analgesia and supplemental sedative effects while the patient remains intubated in the early postoperative period. Judicious opioid use minimizes or avoids prolonged intubation due to excessive sedation and respiratory depression [84]. Postoperative nausea and vomiting are promptly treated. Other adverse effects of opioids include ileus, particularly when used at higher doses. (See "Postoperative care after cardiac surgery", section on 'Opioids'.)

•Nonopioid analgesics (eg, acetaminophen, dexmedetomidine, ketamine) are used during and after cardiothoracic surgical procedures to minimize opioid dosing. (See "Postoperative care after cardiac surgery", section on 'Nonopioid systemic analgesics'.)

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 dissection and other acute aortic syndromes" and "Society guideline links: Aortic and other peripheral aneurysms".)

SUMMARY AND RECOMMENDATIONS

●Preanesthetic assessment – This includes:

•Assessment of risks – Patient-specific and procedure-specific risks include spinal cord ischemia causing lower extremity paraparesis/paraplegia, cardiovascular events (eg, stroke, myocardial infarction, death), and renal dysfunction. (See 'Risk assessment' above.)

•Review of the surgical plan – Planned interventions to protect the spinal cord and other organs (eg, use of partial left heart bypass, systemic hypothermia, or intrathecal catheter insertion to monitor cerebrospinal fluid [CSF] pressure with drainage of CSF to lower CSF pressure) are discussed with the surgical team. (See 'Review of the surgical plan' above.)

•Review of preoperative tests – Typically, typing and cross-matching of six units of red blood cells (RBCs), six units of fresh frozen plasma, and one unit of platelets is performed; these blood products should be available prior to surgical incision. (See 'Review of preoperative tests' above.)

●Monitoring

•Standard and temperature monitors – In addition to standard monitors, an oropharyngeal and bladder catheter temperature probe are continuously monitored to determine upper and lower body temperatures. (See 'Standard monitors' above and 'Temperature monitors' above.)

•Cardiovascular monitors – These typically include (see 'Cardiovascular monitors' above):

-Intra-arterial continuous monitoring of mean arterial pressure (MAP) – Catheters are inserted in the right radial artery to monitor MAP proximal to the thoracic aortic surgical site and in a femoral artery to monitor MAP distal to the site.

-Central venous catheter (CVC) – Large-bore central venous access is necessary for fluid and blood administration, vasoactive drug infusions, and central venous pressure (CVP) monitoring.

-Transesophageal echocardiography (TEE) – We use TEE monitoring of cardiac function and intravascular volume status, and to determine causes of severe hemodynamic instability (eg, during aortic cross-clamping and unclamping), as discussed separately. (See "Intraoperative transesophageal echocardiography for noncardiac surgery" and "Anesthesia for open abdominal aortic surgery", section on 'Hemodynamic management'.)

-Pulmonary artery catheter (PAC) – A PAC is inserted in patients with symptomatic heart failure or pulmonary hypertension.

•Neuromonitoring for spinal cord ischemia – We typically employ motor evoked potentials (MEPs) and/or somatosensory evoked potentials (SSEPs) to continuously assess spinal cord function and immediately treat evidence of spinal cord ischemia (algorithm 1). (See 'Neuromonitoring for spinal cord ischemia' above.)

•CSF pressure – An intrathecal catheter may be inserted at the lumbar level, with planned drainage of CSF fluid to lower CSF pressure when evidence of spinal cord ischemia develops. (See 'Cerebrospinal fluid (CSF) pressure monitoring' above.)

•Cerebral oximetry – If available, cerebral oximetry is employed to detect decreases in cerebral oxygen saturation >10 percent below baseline. (See 'Cerebral oximetry to monitor for cerebral ischemia' above.)

●Anesthetic techniques (See 'Anesthetic techniques' above.)

•Induction – Induction techniques minimize risk of myocardial ischemia by avoiding hypotension, hypertension, and tachycardia, as discussed separately. (See "Anesthesia for noncardiac surgery in patients with ischemic heart disease", section on 'Induction'.)

A double lumen endotracheal tube (DLT) or bronchial blocker is inserted to achieve one lung ventilation, as discussed in other topics. (See "One lung ventilation: General principles" and "Lung isolation techniques".)

•Maintenance – When neuromonitoring is used, we maintain anesthesia with total intravenous anesthesia (TIVA) or a balanced anesthetic technique (eg, a volatile inhalation agent administered at ≤0.5 MAC plus infusions of dexmedetomidine and an opioid). Other centers employ infusions of propofol plus an opioid, and may administer a ketamine infusion as an adjuvant agent to augment MEP and SSEP amplitudes. These regimens allow elicitation of both MEP and SSEP responses (table 5), as discussed separately. (See "Neuromonitoring in surgery and anesthesia", section on 'Anesthetic effects on neuromonitoring'.)

●Hemodynamic management

•Maintenance of proximal MAP – We suggest maintaining MAP at 80 to 100 mmHg during application of the aortic cross-clamp as a strategy to prevent and manage spinal cord ischemia (Grade 2C) (algorithm 1) . If CVP is ≥CSF pressure, preferentially use vasopressor therapy, rather than volume expansion. Further augmentation in 5 mmHg increments up to 110 mmHg may be necessary to treat persistent spinal cord ischemia. (See 'Control of aortic blood pressure' above.)

•Management of aortic cross-clamping and unclamping (see 'Management of aortic cross-clamping and unclamping' above):

-Aortic cross-clamping causes a sudden, large increase in left ventricular (LV) systolic afterload that can lead to myocardial ischemia and/or LV failure with hemodynamic instability (figure 9).

-Removal of the cross-clamp results in a sudden decrease in systemic vascular resistance (SVR), decreased preload, and hypotension (figure 10) [64]. Also, metabolic acidosis and washout of ischemic muscle tissue may result in hyperkalemia, malignant arrhythmias, and cardiac arrest.

●CSF pressure drainage – We suggest CSF drainage to maintain CSF pressure at 10 mmHg during application of the aortic cross-clamp (Grade 2C) (algorithm 1), particularly if neuromonitoring detects evidence of spinal cord ischemia. (See 'Cerebrospinal fluid (CSF) pressure monitoring' above and 'Maintenance of low CSF pressure with CSF drainage' above.)

●Strategies to prevent renal ischemia – In addition to controlling proximal MAP to maintain renal perfusion, strategies to preserve renal function include maintaining optimal intravascular volume status. We do not administer furosemide, mannitol, or dopamine to provide renal protection. (See 'Control of aortic blood pressure' above and 'Strategies to prevent renal and visceral ischemia' above.)

●Management of anticoagulation, bleeding, and hemostasis (see 'Management of anticoagulation, bleeding, and hemostasis' above):

•Unfractionated heparin is administered for systemic anticoagulation before aortic cross-clamping. Our standard protocol for partial left heart bypass includes dosing heparin with an activated clotting time (ACT) target of approximately 250 seconds. After completion of the repair, the effects of heparin are reversed with protamine to achieve hemostasis.

•Prophylactic antifibrinolytic therapy may be selected based on institutional protocols, as discussed in a separate topic. (See "Intraoperative use of antifibrinolytic agents".)

•Autologous salvaged or allogeneic RBCs are transfused as necessary to maintain the hemoglobin level ≥8 g/dL. We employ point-of-care viscoelastic tests of hemostasis to guide decision-making regarding transfusion of fresh frozen plasma, platelets, or fibrinogen concentrate. Details are discussed separately. (See "Intraoperative transfusion and administration of clotting factors".)

●Postoperative pain management – Multimodal pain therapies include regional analgesia (eg, bilateral thoracic paravertebral blocks, or serratus anterior plane (image 1), erector spinae plane (figure 11), pectoral nerve (image 1), or intercostal nerve block (figure 12 and figure 13 and image 2)), IV patient-controlled analgesia (PCA) with an opioid, and nonopioid analgesics (eg, acetaminophen, dexmedetomidine, ketamine). (See 'Early postoperative management' above.)