Abstract
The need for circulatory arrest during surgical clipping of intracranial aneurysms is uncommon given the recent advances in endovascular options and microsurgical techniques. However, intracranial aneurysms that are large, that are located in the posterior circulation, or that have failed conventional therapy may warrant a highly selective patient group to undergo circulatory arrest as the best and possibly only surgical option. Circulatory arrest permits decompression of the aneurysm, allows appropriate corridors during dissection, and facilitates definitive surgical clipping in patients who might not otherwise be candidates for conventional surgical management. While circulatory arrest, and the methods used to achieve it, is complicated and associated with high morbidity and mortality, for some patients the risk of the procedure is favorable to the natural history of large and complicated intracranial aneurysms. This chapter outlines deep hypothermic and adenosine-induced circulatory arrest methodology and their associated anesthesia management.
Keywords
Adenosine-induced circulatory arrest, Aneurysm clipping, Deep hypothermic circulatory arrest, General anesthesia, Intracranial aneurysm
Introduction
Despite the advent of novel endovascular options and the advancement of microsurgical techniques and instruments, a small subset of intracranial aneurysms present a challenge to the neurovascular practitioner. Intracranial aneurysms of large or giant dimensions may be difficult to treat with conventional techniques, as are aneurysms located at the basilar tip, posterior circulation, and other anatomical areas that hinder adequate anatomical exposure for surgical intervention. Furthermore, aneurysms with significant thrombosis or feeder arteries may be unsuitable for conventional treatment without exposing the patient to significant perioperative morbidity and mortality. While alternative surgical treatments such as extracranial to intracranial bypass with indirect clipping, temporary clips, and endovascular stenting has further reduced the number of patients not suitable for conventional therapy, there continues to be a need for circulatory arrest during intracranial aneurysm surgery to facilitate definitive treatment of these aneurysms.
Circulatory arrest offers the advantage of decreasing aneurysm turgidity for clip placement, minimizing the risk of aneurysm rupture, and allowing delicate dissection needed for permanent clip application. In this chapter, two techniques of circulatory arrest currently being utilized in the treatment of intracranial aneurysms will be presented.
Deep Hypothermic Circulatory Arrest
The use of deep hypothermic cardiac arrest (DHCA) in the surgical treatment of intracranial aneurysm was initially reported over 50 years ago. However, due to the complexity of DHCA and cardiopulmonary bypass (CPB), the popularity of this technique waned in favor of advancing microsurgical clipping and endovascular strategies. Renewed interest in DHCA appeared around the turn of the century as improvements in CPB machines and anesthesia techniques allowed the re-exploration of DHCA as an option for surgical management of large or unfavorably located aneurysms. Despite these advances, DHCA is still associated with high morbidity and mortality and currently limited to highly selective patient populations at quaternary hospital centers with specially trained neurosurgeons.
Anesthesia Management
In addition to routine anesthesia screening (history and physical examination, anesthesia history, comprehensive blood studies, etc.), preoperative workup of the patient should include a cardiovascular examination to determine any contraindications to femoral artery catheterization and CPB such as cardiac valve disorders or coronary artery disease. While these conditions should be optimized prior to surgery, the presence of an unsecured intracranial aneurysm may exclude the patient from preoperative therapeutic intervention that often requires prolonged systemic anticoagulation. Detection of significant cardiac valve disease may warrant open sternotomy to safely institute CPB during DHCA for intracranial aneurysms. Other significant comorbidities (hepatic disease, renal dysfunction, chronic obstructive pulmonary disease/asthma, diabetes mellitus) should be optimized prior to the planned surgery. The anesthetic management of patients undergoing intracranial aneurysm repair with DHCA requires a multidisciplinary team approach, with anesthesiology, neurosurgery, cardiothoracic surgery, intensive care, nursing, and perfusionists all playing a vital role in the execution and planning of the procedure. Members of each team and the equipment necessary to safely perform the procedure must be accommodated in the operating room and good communication between the teams established.
The patient is positioned in a supine position with standard American Society of Anesthesiologists’ monitors. Preinduction invasive hemodynamic monitoring is established via radial arterial line. Induction of anesthesia is achieved through intravenous (IV) administration of a sedative/hypnotic agent (propofol, etomidate) with concomitant administration of opioids, lidocaine, and/or benzodiazepines to avoid recall and to minimize sympathetic response to direct laryngoscopy. Tracheal intubation is assisted with the use of a nondepolarizing muscle relaxant. Maintenance of anesthesia is achieved with a balanced regimen of low-minimum alveolar concentration volatile gas and IV infusion of opioids to avoid rises in ICP from increased cerebral blood flow and to optimize surgical conditions.
Given the complexities and management demands of CPB, central venous access and placement of a pulmonary artery catheter is performed. External cardiac pacing pads should also be positioned. The use of transesophageal echocardiography (TEE) is encouraged, as it aids in the proper placement of the venous cannula into the right atrium and provides real-time visualization of cardiac filling and relaxation. A urinary catheter with temperature sensor is placed, along with temperature probes in the nasopharynx, tympanic membrane, or rectum. Additionally, a brain surface temperature probe can be inserted after craniotomy is performed. Scalp electrodes to detect burst suppression by electroencephalogram (EEG) should be positioned and tested prior to start of surgery. The head is pinned and slightly rotated in accordance to the neurosurgical approach while the body is maintained in a position that allows median sternotomy should the need arise. Preparing and draping of the sites for femoral access, median sternotomy, and craniotomy are performed.
After craniotomy, the aneurysm is exposed to the point at which clipping or further decompression is required. Heparin 300–400 IU/kg is centrally administered to achieve an activated coagulation time ≥400 s. Propofol infusion is started and titrated to establish burst suppression on EEG. Further dose of muscle relaxation, opioids, and benzodiazepines are administered to maintain adequate anesthesia during CPB. After access to the femoral artery and vein are achieved, a venous cannula is positioned at the level of the right atrium as confirmed by TEE. Once CPB is initiated, bypass flow rate is maintained at 2.5–3.0 L/min/m to produce a mean arterial pressure of 50–60 mmHg. Cooling is initiated via a cooling blanket and/or active cooling of oxygenated blood through the extracorporeal heat exchanger. Ventricular fibrillation typically occurs around 25°C with spontaneous cardiac asystole occurring at 18–20°C. Alternatively,40–80 mEq of potassium chloride is administered through the PAC once fibrillation occurs to produce cardiac asystole. Circulation arrest is started once the brain temperature reaches 15°C and burst suppression is maintained on EEG. Blood is drained into the venous reservoir to collapse the aneurysm and facilitate clipping or decompression. Securing the aneurysm should occur as quickly as possible to limit safe circulatory arrest time to <45 min. If longer circulatory arrest times are required, intermittent perfusion may be allowed or further dissection can be performed under low-flow CPB until aneurysm clipping is achieved. CPB is then restarted at low flow to assess competency of the clipping and to ensure adequate hemostasis, at which point the flow is increased to 50–60 mmHg. The patient is rewarmed slowly at a rate of 0.2–0.5°C/min to minimize the risk for tissue acidosis and cerebral ischemia. IV sodium nitroprusside may be administered to promote homogeneous rewarming. As the body temperature approaches normothermia, the heart is transcutaneously defibrillated if a spontaneous perfusing rhythm is not present. The patient is then weaned from CPB. Protamine sulfate is given to reverse the heparin, and once coagulation parameters have normalized, the venous and arterial femoral cannulas are removed. Following surgery, the patient should be monitored in intensive care.
Complications
Many of the complications associated with DHCA for the surgical treatment of intracranial aneurysms can be attributed to the complexities of CPB and hypothermia. Hypothermia produces an increase in systemic vasculature resistance while decreasing cardiac contractility resulting in decreased cardiac output exposing the patient to end organ damage. Hypothermia-induced coagulopathies raise the risk of bleeding complications that could be devastating in a patient with a cerebral aneurysm. Additionally, due to the prolonged recovery phase from this extensive procedure, deep vein thrombosis and pulmonary embolisms are common. Cardiac fibrillation during the cooling process may also cause ischemic injury to the myocardium. Additionally, the use of femoral artery and vein catheterization exposes the patient to the risk of vascular injury.
Similar to conventional treatments of intracranial aneurysms, patients undergoing DHCA are at risk for focal ischemic events from either retraction of the neural structures or as the result of permanent clipping. These events might be greater in patients selected for DHCA since their aneurysms are larger or more complicated. Accordingly, DHCA for intracranial aneurysm repair is associated with high morbidity and mortality ( Table 19.1 ). However, given the grave natural history of giant intracranial and posterior circulation aneurysms, DHCA is comparatively a “safer” treatment option for more complicated aneurysms in patients who have failed conventional interventions.
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