C.3. What are the specific considerations for anesthetic management and monitoring of the patient presenting for open TAAA repair?
Answer:
Patients presenting for TAAA repair typically have multiple preexisting comorbid conditions that require careful attention and evaluation, given that open TAAA repair poses a direct and immediate threat to the cardiac, pulmonary, renal, gastrointestinal, and neurologic systems.
Induction: Mitigating aortic wall stress is paramount during induction of anesthesia for patients presenting prior to rupture. A smooth and hemodynamically stable induction of general anesthesia with adequate depth of anesthesia and analgesia prevents hypertension, tachycardia, and increased stress on the aneurysm caused by stimulation during intubation. An awake arterial catheter should be placed for close continuous monitoring of arterial blood pressure with right radial access preferred in the event that the aortic cross-clamp is placed proximal to the LSCA.
Short-acting antihypertensive agents, such asnitroglycerin, nicardipine, esmolol, and labetalol, are useful for maintaining hemodynamic stability. When patients present for an emergent case with possible rupture, the risk of hypotension and malperfusion from bleeding must be balanced with the need to avoid hypertension. Hemodynamic collapse can occur after induction since the tamponade effect is lessened by the relaxation of abdominal vasculature, venous return is decreased with the onset of positive pressure ventilation, and sympathetic tone may be reduced by anesthetic agents. As surgical dissection exposes the aorta, the counterforce to the systemic blood pressure on the aneurysm wall is decreased, increasing the risk of aneurysm rupture. Prior to cross-clamp removal and reperfusion of the visceral organs and lower extremities, systemic blood pressure should be increased because removal of the cross-clamp and reperfusion can lead to profound hypotension.
Airway: Repair of type I, II, and some type III TAAAs requires lung isolation for adequate visualization, which can be accomplished with a double-lumen tube (DLT) or a bronchial blocker. A DLT provides access to the nonventilated lung for suctioning and the addition of continuous positive airway pressure (CPAP) when oxygenation is inadequate. Patients require intubation and mechanical ventilation in the intensive care unit postoperatively due to the need for large-volume resuscitation, correction of coagulopathy, and concern for pulmonary dysfunction, which can result from pulmonary edema, left lung trauma from retraction, diaphragmatic dysfunction, as well as possible phrenic and recurrent laryngeal nerve damage. The use of a bronchial blocker obviates the need to exchange the DLT for a single-lumen endotracheal tube at the conclusion of the procedure in a potentially edematous airway. Also, it can be simpler to place a larger single-lumen tube with a blocker than a DLT. A bronchial blocker is easier to position when large thoracic aneurysms displace or compress the left mainstem bronchus; alternatively, a right-sided DLT might be required since left-sided DLTs may be difficult to place in this circumstance. Lung-protective ventilation should be used regardless of airway technique.
Access: Central venous access with multiple 8.5F or 9F introducers should be obtained with consideration for additional large-bore peripheral access with 8.5F rapid infusion catheter or 14-gauge catheters in anticipation of the need for rapid resuscitation and vasoactive medication delivery. A rapid infusion system, such as the Belmont Rapid Infuser, is used to reinfuse shed blood and ensure timely resuscitation; the rate of flow should be confirmed both before and after positioning. The placement of a pulmonary artery catheter (PAC) can be useful for the optimization of volume status and mitigation of left and/or right heart dysfunction during aortic clamping/unclamping in centers that have expertise in PAC-guided management.
In addition to right radial arterial access, some centers consider simultaneous femoral arterial cannulation to assess perfusion distal to supraceliac cross-clamps and titrate LHB flow rates to optimize visceral, renal, spinal cord, and lower extremity perfusion.
Spinal cord protection: Spinal cord injury with resultant paraplegia remains one of the most serious complications of TAAA repair despite major advances in surgical technique. Temporary occlusion of the aorta with a cross-clamp, sacrificed intercostal arteries, and embolization of air or particulate matter to the aorta may contribute to the development of spinal cord injury. Enhancement of spinal cord perfusion by maximizing oxygen-carrying and delivery capacity with more liberal transfusion triggers (hemoglobin <10 g/dL) is thought to mitigate spinal cord injury, in addition to other techniques described in the sections that follow.
Hypothermia
Mild hypothermia to 32 °C might provide neuronal protection by reducing excitatory neurotransmitter release, decreasing free oxygen radical production, decreasing postischemic edema, and stabilizing central nervous system (CNS) blood flow. A core temperature of 32 °C to 34 °C is achieved via passive heat loss for cases not involving HCA, although active cooling can also be facilitated by heat exchangers on bypass circuits. It is also reasonable to use moderate hypothermia to protect the spinal cord from ischemic injury.
Some centers implement regional hypothermia of the spinal cord using epidural infusion of crystalloid solution at 4 °C in anticipation of aortic cross-clamping. Regional hypothermia might help avoid the detrimental effects of systemic hypothermia on the coagulation system. Epidural cooling can be instituted with the insertion of a T12-L1 epidural catheter and an L3-L4 intrathecal thermistor catheter, selectively cooling the spinal cord after aortic cross-clamp. The spinal cord is cooled at the T8-L1 region, a watershed area with variation in collateral blood supply most susceptible to ischemic injury. The thermistor catheter allows the measurement of temperature and cerebrospinal fluid (CSF) pressure. After full TAAA reconstruction is completed, epidural cooling is stopped. However, there is currently no data to support superior outcomes with regional hypothermia as compared to systemic hypothermia.
Cerebrospinal Drainage
CSF drainage in the perioperative period is the only technique with strong evidence to support a reduction in spinal cord injury in open and endovascular thoracic aortic repairs. During aortic cross-clamp and surgical retraction, CSF pressure can acutely increase due to a rise in venous pressure and a corresponding CSF pressure rise, which causes a decrease in spinal cord perfusion pressure (SCPP). Furthermore, the spinal cord can become edematous due to reperfusion injury. Lumbar drains are placed into the intrathecal space below the L2-L3 level preoperatively in hemodynamically stable patients and at the completion of the procedure in unstable patients to mitigate the rise in CSF pressure. CSF is drained to maintain a CSF pressure less than 10 to 15 mm Hg, without exceeding a maximal drainage rate of 10 to 15 mL/h. Careful titration may be necessary to permit more drainage if perfusion pressure drops, but at an elevated risk of subdural hematoma from tearing of bridging dural veins, especially when CSF pressure is less than 5 mm Hg. SCPP is estimated as the difference between the MAP and the CSF pressure. Therefore, measures that increase MAP and decrease CSF pressure result in improved spinal cord perfusion. It is reasonable to target a MAP of 85 to 100 mm Hg and an SCPP greater than or equal to 70 mm Hg.
Other pharmacologic strategies to decrease the risk of paraplegia and enhance spinal cord protection have been trialed without evidence to support improved outcomes. Such interventions include intrathecal papaverine, naloxone to reduce excitatory neurotransmitter release, and steroids to mitigate neuronal excitotoxicity, stabilize neuronal membranes, and decrease edema.
Neuromonitoring
Neuromonitoring of somatosensory evoked potential (SSEP) and motor evoked potential (MEP) can be utilized for timely diagnosis of ischemia and modification of surgical technique when ischemia occurs. SSEPs monitor the integrity of the dorsal column of the spinal cord while MEPs monitor the function of the corticospinal tract and anterior horn motor neurons. Use of MEPs necessitates the use of a total IV anesthetic, in addition to avoidance of paralysis, while the use of SSEP requires limitation of volatile anesthetic concentration to 0.5 minimum alveolar concentration (MAC). Although SSEPs are less sensitive to anesthetics and paralytics compared with MEPs, their utility is limited since revascularization of segments with associated SSEP changes ultimately did not affect the incidence of postoperative neurologic injury. Increased latency or decreased amplitude of MEPs is associated with paraplegia, which should prompt a higher MAP goal, increased CSF drainage, movement of the cross-clamp to improve perfusion of the intercostal arteries, and reimplantation of critical intercostal arteries. The use of neuromonitoring is supported by some institutions but is not a standard, widespread practice. Some institutions will institute a wake-up test prior to transportation to the ICU, during which the patient is asked to move their lower extremities. After completion of the wake-up test, the patient is reanesthetized.
The use of near-infrared spectroscopy (NIRS) along the paravertebral muscles for noninvasive surveillance of real-time spinal oxygenation and perfusion has been introduced but requires further investigation in human studies prior to routine clinical implementation. A pilot study validated the association between regional hemoglobin oxygen saturation using NIRS and MEP monitoring, in addition to demonstrating the feasibility of NIRS to surveil the hemodynamic changes in oxygenation of the paraspinal region during and after TAAA repair.
Left-Heart Bypass
LHB is commonly used to provide distal aortic perfusion during the period of aortic cross-clamp, as described in the previous sections (Figure 9.14).
Hemodynamic considerations for left-heart bypass and aortic cross-clamping: In anticipation of proximal aortic cross-clamping, LHB flow is initiated at 0.5 L/min and then gradually increased to 1 to 2.5 L/min once the cross-clamp is in place to maintain a MAP of 85 to 100 mm Hg. Careful assessment of arterial pressure is crucial as flow via the LHB circuit is increased since flow and perfusion can simultaneously be decreased to organs above the cross-clamp. The more proximal the aortic clamp, the more extreme the augmentation of blood pressure can be due to an increase in afterload. Nicardipine, nitroglycerin, nitroprusside, and the vasodilating properties of inhaled volatile can be used to help offset the increase in afterload seen with aortic cross-clamping. An increase in preload or central hypervolemia, manifested by increases in filling pressures, is also seen due to a decrease in venous capacitance that shifts blood away from vascular beds below the cross-clamp and toward the vasculature proximal to cross-clamp. Nitroglycerin-mediated venodilation helps mitigate the amplification in blood pressure that results from a reduction in venous capacity and permits volume expansion in anticipation of the central hypovolemia that will ensue with cross-clamp removal.
Once the distal anastomosis is completed, the aortic cross-clamp is slowly removed to reestablish blood flow to the lower body. The hypotension that ensues with cross-clamp release requires treatment with infusion of vasopressor medications and sodium bicarbonate to counteract the metabolic acidosis that results from the accumulation of vasoactive and myocardial-depressant metabolites in hypoperfused tissues that become released upon cross-clamp removal. Sodium bicarbonate can be administered as an infusion at 1 to 2 mg/kg/h during the cross-clamp period. The hypotension can also be combated with volume loading. Intermittent partial reapplication of the cross-clamp may be necessary to provide time for pharmacologic elevation of systemic vascular resistance (SVR), volume replacement, and reversal of metabolic acidosis with sodium bicarbonate.
A higher blood pressure than normal (MAP > 85 mm Hg) is typically maintained after cross-clamp release to ensure adequate renal and spinal cord perfusion. However, the blood pressure goal might be dependent on the complexity of the repair, as there are multiple suture lines prone to bleeding, as well as the fragility of aortic tissue in patients with heritable pathology.
References
- Boezeman RP, van Dongen EP, Morshuis WJ, et al. Spinal near-infrared spectroscopy measurements during and after thoracoabdominal aortic aneurysm repair: a pilot study. Ann Thorac Surg. 2015;99:1267-1274.
- Cambria RP, Davison JK, Carter C, et al. Epidural cooling for spinal cord protection during thoracoabdominal aneurysm repair: a five-year experience. J Vasc Surg. 2000;31:1093-1102.
- Chatterjee S, Preventza O, Orozco-Sevilla V, Coselli JS. Perioperative management of patients undergoing thoracic endovascular repair. Ann Cardiothorac Surg. 2021;10:768-777.
- Gelman S. The pathophysiology of aortic cross-clamping and unclamping. Anesthesiology. 1995;82:1026-1060.
- Lester LC, Kostibas MP. Anesthetic management for open thoracoabdominal and abdominal aortic aneurysm repair. Anesthesiol Clin. 2022;40:705-718.