INTRODUCTION — Open surgical repair of the descending thoracic aorta is used to manage thoracic aortic pathology such as aneurysm, dissection, or injury in selected patients. Despite advances in surgical, perfusion, and anesthetic techniques, mortality and significant morbidity may occur during open repair due to ischemia that can affect the brain, spinal cord, kidney, viscera, and extremities.
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. (See "Overview of open surgical repair of the thoracic aorta", section on 'Descending aorta' and "Endovascular repair of the thoracic aorta".)
This topic will review anesthetic management for patients undergoing open surgical repair of the descending thoracic aorta. Separate topics review anesthetic management of patients undergoing endovascular aortic procedures or open surgical repair of other aortic segments (eg, the abdominal aorta, ascending aorta, aortic arch):
●(See "Anesthesia for endovascular aortic repair".)
●(See "Anesthesia for open abdominal aortic surgery".)
●(See "Anesthesia for aortic surgery requiring deep hypothermia".)
PREANESTHETIC ASSESSMENT — The preanesthetic consultation includes assessment of patient-specific and procedure-specific risks, the planned surgical approach, and interventions that are likely to prevent or ameliorate adverse outcomes.
Assessment of risks and risk reduction strategies — Perioperative morbidity and mortality after thoracic aortic surgery is high compared with most elective surgical procedures due to potential for ischemia and embolic complications, large blood loss, and prolonged duration of surgery [1]. Preoperative functional status is a prognostic factor for perioperative mortality, with a threefold difference between independent and completely dependent patients [2]. Female sex is also associated independently with an increased risk of mortality and stroke after thoracic aortic surgery [3].
Paraparesis/paraplegia — The reported risk of spinal cord ischemia following open repair of thoracoabdominal aortic aneurysm or dissection resulting in paraparesis or paraplegia has ranged from 2 to 25 percent [1,4]. Improvements in surgical and anesthetic techniques have reduced this risk to 1 to 6 percent (comparable to the 4 to 7 percent risk reported for endovascular repair) [1,5-7]. A 2020 meta-analysis that included 22,634 patients (169 studies) undergoing aortic aneurysm repair noted that an overall incidence for permanent spinal cord ischemia (SCI) of 4.5 percent (95% CI 3.8-5.4); 5.7 percent (95% CI 4.3-7.5) for open repair and 3.9 percent (95% CI 3.1-4.8) for endovascular repair [8]. In that study, the incidence of SCI was higher for thoracoabdominal aneurysm repair (7.6 percent) compared with descending aortic aneurysm repair (3.5 percent). Other studies have also noted that the location, extent, and effect of thoracic aortic pathology on spinal cord vascular supply determine the risk of spinal cord ischemia [9-11]. (See "Spinal cord infarction: Epidemiology and etiologies", section on 'Vascular anatomy'.)
Surgical procedures that include replacement or coverage of a large aortic segment are associated with the highest risk (eg, from the distal left subclavian artery to below the renal artery). One surgical strategy for spinal cord protection during thoracic aortic surgery is preservation of flow to the dominant anterior radicular artery that supplies the spinal cord (ie, the arteria radicularis magna, also known as the artery of Adamkiewicz), which may arise anywhere from T7 to L2 level [12] (see 'Surgical adjunctive techniques' below). In addition, the subclavian artery, segmental intercostal and lumbar arteries, internal iliac artery, and the perivertebral capillary network each contribute to normal spinal cord perfusion [4,13,14].
Furthermore, physiologic reserves for perfusion exist via the spinal cord collateral networks, and collateral blood flow may be the main determinant of spinal cord perfusion [4,14]. During a period of thoracic aortic cross-clamping, perfusion of the spinal cord is variable and tenuously dependent upon this collateral circulation [10]. If disruption of arterial feeder flow is significant or prolonged (eg, during temporary interruption of spinal cord blood supply during the intraoperative period or as a consequence of a permanent reduction in blood supply due to ligation or coverage of critical blood vessels in a patient with inadequate collateral blood flow), consequential spinal cord ischemia and persistent injury may occur [4,14].
Surgical and anesthetic strategies to prevent and treat perioperative spinal cord ischemia are discussed below. (See 'Spinal cord protection' below.)
Cardiovascular complications — Patients with aortic vascular 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) [1,15,16]. 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 preexisting cerebrovascular disease and the potential for embolism of aortic atherosclerotic debris into the cerebral circulation during surgical manipulation of the aortic arch [1,17-19].
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 [4], with the goal of maintaining cerebral perfusion and ensuring that spinal cord perfusion pressure is at least 70 mmHg, which has been associated with a decreased risk of spinal cord ischemia and injury [20]. This may be particularly important in patients with longstanding hypertension that may have caused a shift in the cerebral autoregulation threshold [21]. (See "Anesthesia for patients with hypertension".)
Renal dysfunction — During thoracic aortic surgery, 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, which is associated with worse outcomes after surgery [22-25]. Specifically, mild acute kidney injury is associated with increased in-hospital mortality, while moderate to severe acute kidney injury is also associated with increased long-term mortality risk [26]. Other studies have noted that elevated preoperative serum creatinine is a predictor of postoperative renal dysfunction after either abdominal or thoracic aortic surgery (table 1) [22,27,28].
Routine strategies to preserve renal function during vascular surgery include ensuring adequate preoperative hydration and maintaining optimal intravascular volume status and hemodynamic stability throughout the perioperative period. Specific surgical strategies for patients undergoing open repair of the descending thoracic aorta are discussed below. (See 'Renal and visceral protection' below.)
Review of the surgical plan — Preoperative review of the surgical approach is necessary to plan anesthetic care [4,14]. (See "Overview of open surgical repair of the thoracic aorta", section on 'Preoperative evaluation and preparation'.)
Examples include:
●Planned use of partial left heart bypass for distal aortic perfusion and/or selective perfusion of renal, segmental, and/or mesenteric arteries affects selection of intra-arterial monitoring sites. (See 'Partial left heart bypass' below.)
●Planned use of systemic hypothermia guides selection of temperature monitoring sites and warming devices. (See 'Systemic hypothermia' below.)
●The decision to insert an intrathecal catheter is based on indications for monitoring cerebrospinal fluid (CSF) pressure and plans to drain CSF to lower this pressure if spinal cord ischemia become evident during neuromonitoring. (See 'Cerebrospinal fluid (CSF) pressure monitoring and drainage' below and 'Cerebrospinal fluid (CSF) drainage' below and 'Neuromonitoring for spinal cord ischemia' below.)
Review of laboratory tests — 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.
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".)
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 (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 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".)
●Prophylactic antibiotics – Administration of the selected prophylactic antibiotic(s) within the recommended timeframe minimizes infection risk (table 3).
INTRAOPERATIVE ANESTHETIC MANAGEMENT
Monitoring
Standard monitors — All patients have standard noninvasive monitoring, including electrocardiography (ECG), pulse oximetry (SpO2), and intermittent noninvasive blood pressure (BP) cuff measurements (table 4).
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'.)
A bladder catheter is inserted after induction to measure urine output.
Cardiovascular monitors
●Proximal and distal intra-arterial catheters – We insert two intra-arterial catheters for continuous monitoring of arterial BP; a catheter for monitoring proximal BP is inserted in the right radial artery. This is typically accomplished before induction in order to detect and optimally treat hypertension or hypotension that may occur during administration of anesthetic induction agents, laryngoscopy, and endotracheal intubation. Also, an intra-arterial catheter to monitor distal BP is inserted in a femoral artery, typically after induction. Patients with thoracic aortic aneurysm often have peripheral arterial atherosclerosis and may have discrepancies in BP between upper versus lower extremities and right versus left upper extremities.
Maintenance of adequate mean arterial pressure (MAP) is particularly critical in patients with high risk for paraparesis/paraplegia, and MAP is incrementally increased if evidence of spinal cord ischemia develops (table 5) [29-34]. (See 'Control of proximal aortic blood pressure' below.)
Intra-arterial catheters are also used for evaluation of respirophasic variations in the arterial pressure waveform (figure 1) (see "Intraoperative fluid management", section on 'Dynamic parameters to assess volume responsiveness'), as well as for intermittent blood sampling for laboratory tests. (See 'Point-of-care laboratory testing' below.)
●Central venous catheter and intravascular access – We insert a dual port central venous catheter (CVC) in an internal jugular vein to provide large-bore 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 [35-39]. (See "Intraoperative fluid management", section on 'Traditional static parameters'.)
Either a rapid infusion catheter or two large bore peripheral intravascular catheters (IVs) may be inserted to provide additional intravascular access if large blood losses are anticipated.
●Pulmonary artery catheter – We typically insert a pulmonary artery catheter (PAC) if the patient has a history of symptomatic heart failure or pulmonary hypertension.
●Transesophageal echocardiography – Similar to patients undergoing open abdominal aortic surgery, we employ transesophageal echocardiography (TEE) to monitor cardiac function and intravascular volume status during open thoracic aortic surgery, with the goal of avoiding and/or treating episodes of severe hemodynamic instability, particularly during aortic cross-clamping and unclamping. (See "Anesthesia for open abdominal aortic surgery", section on 'Hemodynamic management'.)
Specifically, TEE monitoring is used to avoid hypovolemia or hypervolemia, detect regional and global ventricular dysfunction (figure 2 and figure 3), and determine causes of hypotension. Thoracic 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 (movie 1) [40-46]. 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. Early recognition of myocardial ischemia or ventricular dysfunction facilitates management. (See "Intraoperative transesophageal echocardiography for noncardiac surgery", section on 'Volume status' and "Intraoperative transesophageal echocardiography for noncardiac surgery", section on 'Ventricular function' and 'Partial left heart bypass' below.)
TEE is also used to detect aortic pathology such as atheromas, thromboembolism, air embolism, or aortic dissection resulting from cannulation or cross-clamping of the aorta. Even if TEE is not used electively, rapid deployment may be urgently needed to diagnose causes of 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 initiating interventions to immediately treat evidence of spinal cord ischemia to avoid irreversible injury (table 5) [4,14,47]. (See "Neuromonitoring in surgery and anesthesia", section on 'Motor evoked potentials' and "Neuromonitoring in surgery and anesthesia", section on 'Somatosensory evoked potentials'.)
Motor evoked potentials (MEPs) — Transcranial monitoring 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 4). Transesophageal stimulation MEPs may be a feasible alternative to transcranial stimulation [48]. (See "Neuromonitoring in surgery and anesthesia", section on 'Motor evoked potentials'.)
MEP monitoring has implications for anesthetic management including (table 6) [49-51] (see "Neuromonitoring in surgery and anesthesia", section on 'MEP monitoring'):
●Need for total intravenous anesthesia (TIVA) technique or an alternative balanced technique that includes only a low dose of a volatile inhalation agent during the period that MEPs are being monitored. We typically employ an infusion of dexmedetomidine (see "Maintenance of general anesthesia: Overview", section on 'Dexmedetomidine') [52], together with an opioid infusion (typically sufentanil (see "Perioperative uses of intravenous opioids: Specific agents", section on 'Sufentanil')), and a volatile inhalation agent administered at ≤0.5 minimum alveolar concentration (MAC) value (table 7) (see "Inhalation anesthetic agents: Clinical effects and uses", section on 'MAC and MAC-awake values for inhalation agents'). In most patients, this regimen allows elicitation of both MEP and SSEP responses. In other institutions, TIVA is achieved with infusions of propofol plus an opioid (eg, fentanyl, sufentanil, remifentanil).
●Avoidance of neuromuscular blocking agents (NMBAs).
●Avoidance of volatile inhalation anesthetic concentrations ≥0.5 MAC to avoid diminishing the amplitude of MEP responses to the extent that they would be undetectable [53]. Nitrous oxide (N2O) is also avoided due to its similar effects on MEPs, as well as additive effects when N2O is coadministered with a volatile anesthetic agent [54,55].
●In some cases, a ketamine infusion is used as an adjuvant agent to augment MEP amplitude (as well as SSEP amplitude) [56,57]. Since ketamine has anesthetic and analgesic effects, the doses of other anesthetic agents may be reduced [58]. (See "Maintenance of general anesthesia: Overview", section on 'Ketamine'.)
Limitations of MEP monitoring for spinal cord ischemia include the following caveats:
●Reversible intraoperative changes do not correlate with paraplegia [59,60].
●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 [60,61]. However, MEPs <25 percent of control values are not necessarily associated with severity of spinal cord damage [61].
●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) [62-64]. (See 'Systemic hypothermia' below.)
●Interpretation of MEPs may be challenging since intraoperative changes that may indicate ischemia are not standardized [59].
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 in order to monitor continuity of lateral and posterior column function (figure 5). (See "Neuromonitoring in surgery and anesthesia", section on 'Somatosensory evoked potentials'.)
SSEP monitoring has implications for anesthetic management including (table 6) [49-51]:
●Selection of a TIVA technique or an alternative balanced technique that includes only a low dose of a volatile inhalation agent (≤0.5 MAC), as noted above for neuromonitoring of MEPs (see 'Motor evoked potentials (MEPs)' above). Higher doses of volatile inhaled anesthetic agents and administration of N2O are avoided since these delay conduction time and decrease amplitude of SSEPs. (See "Neuromonitoring in surgery and anesthesia", section on 'SSEP Monitoring'.)
●A ketamine infusion may be employed as an adjuvant agent to augment SSEP amplitude, similar to its effect on the amplitude of MEP potentials, and its use allows reduction of the doses of other anesthetic agents [56,57]. (See "Maintenance of general anesthesia: Overview", section on 'Ketamine'.)
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 [5].
●Hypothermia can delay conduction time and decrease amplitude, creating a false positive response that appears similar to ischemic SSEP changes [63,64]. (See 'Systemic hypothermia' below.)
Cerebrospinal fluid (CSF) pressure monitoring and drainage — CSF pressure is monitored in patients with high risk for paraparesis/paraplegia such as previous aortic surgery, stenting, or extended aortic segment coverage (figure 6), in conjunction with drainage of CSF to lower CSF pressure and improve spinal cord perfusion pressure when evidence of spinal cord ischemia develops (table 5) [4,14,29-34]. (See 'Cerebrospinal fluid (CSF) drainage' below.)
The technique involves insertion of a lumbar intrathecal catheter into the subarachnoid space at the level of the L3-L4 disc. In some centers, the intrathecal catheter is inserted on the day before surgery 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 [65]. In other centers, the intrathecal catheter is inserted in the operating room by the anesthesiologist immediately before induction of general anesthesia. The 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.
Candidates for CSF pressure monitoring and drainage include those with known preoperative and/or likely intraoperative risk factors for spinal cord ischemia including [29-34]:
●Need for open surgical and/or endovascular repair in a patient with Crawford class II aneurysm extent (figure 7)
●Planned hybrid surgical approach (ie, open repair plus an endovascular stent) for more extensive coverage of a Crawford class I to III aneurysm extent (figure 8)
●Planned endovascular coverage of the left subclavian segment without revascularization to the left upper extremity in a patient with Crawford class I aneurysm extent (figure 9)
●Planned thoracic aortic procedure in a patient with previous thoracic or more distal (ie, abdominal) aortic surgery
●Likelihood of a prolonged aortic cross-clamp time for any reason
●Emergency surgery (if time permits)
In a meta-analysis of three randomized trials in patients undergoing elective or emergency open repair of thoracic or thoracoabdominal aortic aneurysm (289 patients), lower limb paraparesis or paraplegia occurred in 12 percent of the patients who underwent CSF drainage when indicated, compared with 33 percent of those without CSF drainage (pooled odds ratio [OR] 0.3; 95% CI 0.17-0.54) [66]. Similarly, in a meta-analysis of five cohort studies including 854 patients, lower limb neurologic deficits were noted in 5.4 percent of patients who had CSF drainage versus 15 percent in those who did not (pooled OR 0.3; 95% CI 0.17-0.54) [66].
There are risks associated with intrathecal catheter placement for CSF drainage. In a systematic review of 4714 patients undergoing either open or endovascular repair of thoracic or thoracoabdominal aortic pathology (34 studies), severe drainage-related 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; and 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 [67]. Mortality related to CSF drainage was reported to be 0.9 percent.
Cerebral oximetry — 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); thus, the surgeon is notified immediately [68].
If a bilateral (presumably global) decrease in cerebral oxygen saturation is >10 percent compared with baseline, efforts to increase oxygen delivery may include [19]:
●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
Temperature monitoring — An oropharyngeal temperature probe and the bladder catheter temperature probe are continuously monitored to determine upper body and lower body temperatures with or without partial left heart bypass (see 'Partial left heart bypass' below). Temperature monitoring is particularly important during and after a period of deliberate systemic hypothermia, because normothermia should be reestablished and maintained during the remainder of the procedure. (See 'Systemic hypothermia' below.)
Point-of-care laboratory testing — Point-of-care (POC) testing during open aortic surgery includes arterial blood gases and pH, hemoglobin, electrolytes, glucose, as well as activated clotting time (ACT) if anticoagulation with heparin is employed. Our standard protocol with left heart bypass includes dosing heparin with a goal ACT of approximately 250 seconds. After cessation of left heart bypass, we reverse the effects of heparin with protamine [69]. If available, POC tests of hemostasis (eg, thromboelastography [TEG] or rotational thromboelastometry [ROTEM]) are employed if there are clinical signs of coagulopathy or significant bleeding [70]. (See "Clinical use of coagulation tests", section on 'Point-of-care testing'.)
Induction and airway management — Techniques for induction of general anesthesia should minimize risk of myocardial ischemia, with avoidance of hypotension, hypertension, and tachycardia. (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 if aortic dissection or cross-clamping above the diaphragm is necessary. (See "One lung ventilation: General principles" and "Lung isolation techniques".)
Prevention and management of coagulopathy — In some centers, prophylactic antifibrinolytic therapy (either a lysine analog such as epsilon-aminocaproic acid or tranexamic acid) is administered to decrease the risk of perioperative bleeding [1]. (See "Perioperative blood management: Strategies to minimize transfusions", section on 'Antifibrinolytic agents'.)
RBCs are transfused as necessary to maintain the hemoglobin level ≥8 g/dL or >9 g/dL in patients with significant ongoing bleeding or evidence of myocardial or other organ ischemia. We employ POC tests of hemostasis (eg, TEG or 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) [71]. (See "Intraoperative transfusion of blood products in adults", section on 'Indications and risks for specific blood products' and "Intraoperative transfusion of blood products in adults".)
Maintenance — If neuromonitoring is planned, we typically employ a balanced technique to maintain anesthesia, with infusions of dexmedetomidine and an opioid, as well as a volatile inhalation anesthetic agent administered at ≤0.5 MAC, as noted above. (See 'Motor evoked potentials (MEPs)' above and 'Somatosensory evoked potentials (SSEPs)' above.)
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 [15,16]. 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 [72-75]. (See "Anesthesia for noncardiac surgery in patients with ischemic heart disease", section on 'Maintenance'.)
Emergence — 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. These patients are transported to the intensive care unit (ICU) for a period of postoperative controlled ventilation.
SPINAL CORD PROTECTION
General principles for spinal cord protection — Surgical strategies to protect the spinal cord during descending thoracic aortic surgery include use of partial left heart bypass, systemic hypothermia, and/or other adjunctive techniques such as selective perfusion or reimplantation of segmental spinal arteries. (See 'Partial left heart bypass' below and 'Systemic hypothermia' below and 'Surgical adjunctive techniques' below.)
If changes indicating spinal cord ischemia are noted during neuromonitoring of motor evoked potentials (MEPs) and/or somatosensory evoked potentials (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 (table 5). (See "Neuromonitoring in surgery and anesthesia", section on 'Managing electrophysiologic changes'.)
Specific surgical and anesthetic interventions for preventing and managing spinal cord ischemia are described below. (See 'Surgical interventions' below and 'Anesthesiologist's interventions' below.)
Surgical interventions
Partial left heart bypass — The primary goal of partial left heart bypass is to maintain distal aortic and spinal cord perfusion to the iliolumbar and pudendal arteries and the collateral network complex during the period of aortic cross-clamping [14]. Several methods for cardiopulmonary bypass have been described. (See "Overview of open surgical repair of the thoracic aorta", section on 'Descending aorta'.)
Partial left heart bypass also allows beneficial unloading of the left ventricle during aortic cross-clamping to prevent excessive proximal hypertension, and provides perfusion of the kidneys, mesentery, and lower extremities. Furthermore, systemic temperature can be controlled by adding a heat exchanger to the partial left heart bypass perfusion circuit, allowing induction of mild hypothermia. (See 'Systemic hypothermia' below.)
Typically, mean arterial pressure (MAP) is maintained ≥80 mmHg for 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) during partial left heart bypass.
At our institution, partial left heart bypass is typically employed at the discretion of the surgeon, particularly if a long aortic cross-clamp time is anticipated. It is unclear whether partial left heart bypass can improve spinal cord perfusion sufficiently to prevent paraparesis/paraplegia. Some retrospective studies have noted reduced paraplegia and other benefits [76-79], with reduced 30-day mortality and overall postoperative morbidity in the largest of these studies [79]. However, not all studies have shown reduction in the incidence of paraplegia with partial left heart bypass compared with a simple "clamp and sew" technique (ie, aortic cross-clamping and expeditious surgery without partial bypass) [80].
Systemic hypothermia — For surgical repair of the descending thoracic aorta, permissive hypothermia to approximately 34 degrees Celsius is typically allowed prior to aortic cross-clamping if either partial left heart bypass (see 'Partial left heart bypass' above) or the 'clamp-and-sew' technique is employed [14]. In some centers, mild hypothermia is induced with the aid of a heat exchanger incorporated in the perfusion circuit during partial left heart bypass [5,14].
Hypothermia protects against neuronal injury in the brain or spinal cord by decreasing neuronal oxygen consumption and metabolic rate, thereby promoting tolerance to ischemia. Cerebral oxygen consumption (CMRO2) decreases by a factor of 2.3 for every 10°C decrease in body temperature (figure 10). Also, it is likely that hypothermia has protective actions independent of its effect on cerebral metabolism, including attenuation of release of excitatory neurotransmitters and inflammatory mediators and prevention of neuronal apoptosis after ischemic injury. Notably, neuroprotection during aortic surgery involving the ascending aorta or arch is effectively accomplished with full systemic cardiopulmonary bypass and elective deep hypothermia (<28°C) with circulatory arrest (DHCA), as discussed separately. (See "Anesthesia for aortic surgery requiring deep hypothermia", section on 'Cardiopulmonary bypass with deep hypothermic circulatory arrest'.)
Adverse perioperative effects associated with induced hypothermia include increased risk of coagulopathy, cardiac arrhythmias, hyperglycemia, and decreased metabolism of anesthetic agents and other drugs (table 8). Also, hypothermia may mask or eliminate responses to both MEPs and SSEPs. Furthermore, there is a wide variation in recovery of MEP amplitude during rewarming after a period of DHCA, so that it may be difficult to determine whether lower extremity motor function is intact [81]. (See "Neuromonitoring in surgery and anesthesia", section on 'Temperature'.)
Rewarming after a hypothermic period must be accomplished gradually, with care to avoid systemic hyperthermia. This is typically accomplished by warming of all intravenous fluids, irrigating the thorax with warmed saline, and use of a forced-air warming blanket. Some centers use a heat exchanger in the partial left heart bypass perfusion circuit [5].
Surgical adjunctive techniques — Surgical adjunctive techniques to avoid or treat spinal cord ischemia include selective perfusion of segmental intercostal and lumbar arteries with cold crystalloid or blood [77,82-84], and/or reimplantation of the thoracic intercostals (typically as a patch) that are supplying the arteria radicularis magna (ie, artery of Adamkiewicz) or other vessels that may provide critical spinal cord blood supply (figure 11) [5,85-89]. Although selective perfusion was associated with an increased risk of paraplegia in one case series of 3309 patients, this association was likely due to use of this technique in higher-risk extensive procedures [90]. (See "Overview of open surgical repair of the thoracic aorta", section on 'Descending aorta'.)
Anesthesiologist's interventions
Control of proximal aortic blood pressure — Proximal aortic blood pressure control by the anesthesiologist aims to keep MAP ≥80 mmHg using vasopressors or fluid administration, in order to maintain adequate spinal cord perfusion and prevent or treat spinal cord ischemia noted with neuromonitoring [4,5,14,21]. The goal for proximal aortic MAP is ≥80 mmHg, whether the surgeon employs partial left heart bypass or simply cross-clamps the thoracic aorta without use of partial bypass (ie, "clamp and sew" technique). Patients with longstanding preexisting hypertension have a particularly high risk for development of spinal cord ischemia with resultant paraparesis/paraplegia and may need further augmentation of MAP to restore spinal cord perfusion [91]. 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 (table 5).
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 'Cerebrospinal fluid (CSF) drainage' below). These goals will ensure that spinal cord perfusion pressure (SCPP) is ≥70 mmHg according to the following formula:
SCPP = MAP - CSF pressure
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 [10]. Connections between these vessels open and close dynamically to maintain compensatory flow, depending on the relative pressure in each vessel bed. 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 [21,32,92,93].
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 PaO2 (measured with arterial blood gases), as well as adequate Hgb levels (≥8 g/dL) [94].
Cerebrospinal fluid (CSF) drainage — Intrathecal CSF pressure monitoring with CSF drainage is frequently employed to maintain low CSF pressure (ie, 8 to 10 mmHg) to achieve optimal spinal cord protection [4,5,14,29-34,95,96]. (See 'Cerebrospinal fluid (CSF) pressure monitoring and drainage' above.)
In a 2016 meta-analysis, CSF drainage was effective for preventing neurologic injury (10 studies; 2103 patients), reducing the risk of spinal cord ischemia (SCI) following thoracoabdominal aortic aneurysm (TAAA) repair by nearly one-half (odds ratio [OR] 0.42, 95% CI 0.25-0.7) [97]. 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 [67]. 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 [4,98]. (See 'Control of proximal aortic blood pressure' above and 'Neuromonitoring for spinal cord ischemia' above.)
Guidelines for intrathecal catheter management, CSF pressure monitoring, and CSF drainage include the following:
●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 until pressure is 8 to 10 mmHg.
●Limit CSF drainage to <20 mL during the first hour of surgery.
●Limit CSF drainage to <40 mL during any four-hour period.
●If MEP or SSEP signal amplitudes decrease (indicating ischemia), drain 10 mL of CSF and augment MAP as necessary (table 5) (see 'Control of proximal aortic blood pressure' above).
●If CSF becomes bloody, discontinue drainage immediately and obtain magnetic resonance imaging (MRI) of the spinal cord as soon as feasible.
Intraoperative factors that warrant timely CSF drainage to increase SCPP include [4,32-34,98]:
●Signs of spinal cord ischemia noted with neuromonitoring of MEPs and/or SSEPs (table 5) (see 'Neuromonitoring for spinal cord ischemia' above)
●High CSF pressure >12 to 15 mmHg
●Episodes of hypotension
●Significant backbleeding from segmental arteries (noted in the surgical field)
●Injury to the iliac artery
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 [4,10]. As noted above, an optimal strategy involves both CSF drainage to maintain CSF pressure at 8 to 10 mmHg, as well as maintenance of MAP ≥80 mmHg, thereby ensuring a SCPP ≥70 mmHg (table 5) [4,34] (See 'Control of proximal aortic blood pressure' above.)
RENAL AND VISCERAL PROTECTION — Partial left heart bypass and/or systemic hypothermia during thoracic aortic surgery may avoid or minimize ischemic injury of the kidneys and mesentery, as well as the spinal cord [77]. Another surgical strategy is selective perfusion of the renal and visceral arteries using either cold crystalloid or blood [83,99-101]. However, these techniques have not been evaluated prospectively for efficacy. (See "Overview of open surgical repair of the thoracic aorta", section on 'Descending aorta'.)
Also, the anesthesiologist's efforts to control proximal mean arterial pressure (MAP) will augment perfusion to the kidneys and other abdominal organs. (See 'Control of proximal aortic blood pressure' above.)
Furosemide, mannitol, or dopamine should not be administered solely for the purpose of renal protection, similar to management of patients undergoing open abdominal aortic surgery.
EARLY POSTOPERATIVE MANAGEMENT
Management of postoperative ventilation — Patients are transported to an intensive care unit (ICU) for further monitoring and care after descending thoracic aortic surgery. Most remain sedated and intubated with controlled ventilation for several hours after surgery. After extubation, noninvasive ventilation may be helpful to minimize postoperative pulmonary complications [102].
Management of delayed paraparesis/paraplegia — Continued monitoring of neurologic function, mean arterial pressure (MAP), cerebrospinal fluid (CSF) pressure, and temperature is necessary to recognize and treat postoperative development of paraparesis/paraplegia and other complications [4,14]. Paraparesis/paraplegia due to spinal cord ischemia can present hours or even several days after surgery [103]. Thus, postoperative hourly nursing assessments are performed to detect lower extremity motor weakness until the patient is able to report symptoms of weakness or numbness [33].
If postoperative weakness or paralysis is present in the immediate postoperative period in a patient with normal pulses, urgent management includes the following measures (algorithm 1) [4,14]:
●CSF drainage is employed to lower CSF pressure to 8 to 12 mmHg (see 'Cerebrospinal fluid (CSF) drainage' above). There are several reports of reversal of postoperative paraplegia using this technique [29,104-108].
●MAP is simultaneously increased to augment spinal cord perfusion; typically, the postoperative range is 80 to 100 mmHg [104,105]. (See 'Control of proximal aortic blood pressure' above.)
●Optimal oxygen delivery to the spinal cord is achieved by maintaining cardiac output and optimal O2 content in the blood perfusing the spinal cord, including normal to high hemoglobin (Hgb) saturation (measured with pulse oximetry) and arterial PaO2 (measured with arterial blood gases), as well as adequate Hgb levels (≥8 g/dL).
If there is no evidence of paraparesis or paraplegia, the intrathecal catheter may be clamped (capped) 12 to 24 hours after surgery, and subsequently removed approximately 24 hours after clamping (algorithm 1) [33]. Occasionally, delayed paraplegia/paraparesis occurs after removal of the drainage catheter. In such cases, a new intrathecal catheter is inserted to monitor CSF pressure and drain CSF in an attempt to decompress the intradural compartment and restore spinal cord perfusion, with concurrent maintenance of optimal MAP. In patients with postoperative coagulopathy, the drain may be inserted by a neuroradiologist using fluoroscopic guidance [65].
Avoidance of hyperthermia (ie, fever) throughout the postoperative period is important, since even small increases in systemic temperature may exacerbate ischemic neurologic injury [109]. (See "Spinal cord infarction: Prognosis and treatment".)
Management of postoperative pain — Patients undergoing open thoracic aortic surgical repair have large thoracic or thoracoabdominal incisions causing significant postoperative pain. We manage postoperative pain with intravenous patient controlled analgesia (PCA), typically with the potent opioid sufentanil [110,111]. Regional anesthesia with a local anesthetic administered via bilateral thoracic paravertebral blocks 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 [112-115]. However, placement of a thoracic epidural catheter should be avoided due to the risk of causing an epidural hematoma with compromise of spinal cord blood flow. (See "Management of acute perioperative pain in adults", section on 'Parenteral opioids'.)
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
●The preanesthetic consultation includes assessment of patient-specific and procedure-specific risks for adverse outcomes including:
•Spinal cord ischemia causing lower extremity paraparesis/paraplegia (see 'Paraparesis/paraplegia' above)
•Cardiovascular events (eg, stroke, myocardial infarction, death) (see 'Cardiovascular complications' above)
•Renal dysfunction (see 'Renal dysfunction' above)
•Review of the surgical approach to plan for potential interventions that protect the spinal cord and other organs (eg, planned use of partial left heart bypass, systemic hypothermia, intrathecal catheter insertion to monitor cerebrospinal fluid [CSF] pressure with drainage of CSF to lower CSF pressure, control of proximal aortic blood pressure) (see 'Review of the surgical plan' above)
●In addition to standard monitoring, we typically employ the following cardiovascular monitors (see 'Cardiovascular monitors' above):
•Two intra-arterial catheters for continuous monitoring of arterial blood pressure (BP), including a catheter in the right radial artery inserted before induction to monitor proximal BP, as well as a catheter in a femoral artery inserted after induction to monitor distal BP.
•A central venous catheter (CVC) for large-bore venous access for fluid and blood administration, vasoactive drug infusions, and central venous pressure (CVP) monitoring.
•Transesophageal echocardiography (TEE) to monitor cardiac function and intravascular volume status, due to high risk for severe hemodynamic instability, particularly during aortic cross-clamping and unclamping.
•A pulmonary artery catheter (PAC) if the patient has a history of symptomatic heart failure or pulmonary hypertension.
●Neuromonitoring with motor evoked potentials (MEPs), somatosensory evoked potentials (SSEPs), and cerebral oximetry provides continuous assessment of spinal cord function and cerebral oxygenation during aortic surgery, with the goal of initiating interventions to immediately treat evidence of spinal cord ischemia or cerebral hypoperfusion (table 5). (See 'Neuromonitoring for spinal cord ischemia' above and 'Cerebral oximetry' above.)
●Monitoring of cerebrospinal fluid (CSF) pressure involves insertion of a lumbar intrathecal catheter at the level of the L3-L4 disc, with drainage of CSF fluid to lower CSF pressure if evidence of spinal cord ischemia develops. (See 'Cerebrospinal fluid (CSF) pressure monitoring and drainage' above.)
●Both oropharyngeal and bladder catheter temperature probes are continuously monitored to determine upper and lower body temperatures. (See 'Temperature monitoring' above.)
●Techniques for induction of general anesthesia should minimize risk of myocardial ischemia by avoiding hypotension, hypertension, and tachycardia. A double lumen endotracheal tube (DLT) or bronchial blocker is inserted to achieve one lung ventilation if aortic dissection or cross-clamping above the diaphragm is required. (See 'Induction and airway management' above.)
●If neuromonitoring is planned, maintenance of anesthesia is achieved with a balanced anesthetic technique (eg, a volatile inhalation agent administered at ≤0.5 MAC plus infusions of dexmedetomidine and an opioid) or total intravenous anesthesia (TIVA). High dose volatile inhalation anesthetic agents are avoided during neuromonitoring due to their effects on MEP and SSEP amplitudes. (See 'Maintenance' above.)
●Surgical interventions to prevent ischemia of the spinal cord, mesentery, and kidney during thoracic aortic cross-clamping include use of (see 'Surgical interventions' above):
•Partial left heart bypass (see 'Partial left heart bypass' above)
•Systemic hypothermia (see 'Systemic hypothermia' above)
•Other surgical adjunctive techniques (eg, selective perfusion or reimplantation of segmental intercostal and lumbar, and selective perfusion of renal and visceral arteries) (see 'Surgical adjunctive techniques' above)
●Intraoperative interventions controlled by the anesthesiologist to prevent and treat spinal cord ischemia by improving spinal cord perfusion pressure include (table 5) (see 'Anesthesiologist's interventions' above):
•Maintenance of proximal aortic mean arterial pressure (MAP) at 80 to 100 mmHg, with further augmentation of MAP in 5 mmHg increments up to 110 mmHg if necessary to treat persistent evidence of spinal cord ischemia (see 'Control of proximal aortic blood pressure' above)
•CSF drainage to maintain CSF pressure at 8 to 10 mmHg (see 'Cerebrospinal fluid (CSF) drainage' above)
●Treatment of delayed paraparesis/paraplegia in the postoperative period includes decreasing CSF pressure to 8 to 12 mmHg with CSF drainage and increasing MAP to 90 to 110 mmHg, as well as avoiding hyperthermia (algorithm 1). (See 'Management of delayed paraparesis/paraplegia' above.)
