Hemodynamic Management

One of the most important goals of intraoperative management of neurovascular patients is to maintain adequate cerebral perfusion pressure, thereby preventing secondary cerebral injury due to hypoperfusion (ischemia). In addition, it is important to avoid unnecessary hypertension, which can lead to aneurysmal rupture or perfusion pressure breakthrough (e.g., perilesion edema, resection bed hemorrhage). All anesthetic regimens that maintain patient amnesia/sedation, prevent patient movement in response to noxious stimulation, and provide hemodynamic stability have demonstrated equal safety and efficacy in intracranial surgery.6 The following perioperative events may be associated with transient noxious stimulation that can lead to rapid increases in blood pressure:

1. 
   

   Laryngoscopy and tracheal intubation

   
   
2. 
   

   Placement in Mayfield head fixation

   
   
3. 
   

   Surgical incision

   
   
4. 
   

   Dural traction

   
   
5. 
   

   Brainstem manipulation

   
   
6. 
   

   Placement of brain retractors during posterior fossa and middle fossa surgery

Overly aggressive prophylaxis for treatment of hypertension may lead to unintended hypotension and inadequate cerebral perfusion. Therefore, with the use of ultrarapid offset opioids (e.g., remifentanil or alfentanil) and short-acting vasoactive agents (e.g., esmolol, nicardipine, or nitroprusside), hypertension from these brief, noxious stimuli can be prevented or treated, whereas unintended hypotension is limited in duration and easily corrected. Special consideration should be given to hemodynamic management at the time of temporary occlusion of feeding vessels to facilitate permanent clip placement. To ensure adequate distal cerebral perfusion through collateral vessels, it is necessary to increase mean arterial pressure (MAP) at this time by approximately 20% from baseline values. Once temporary clips are removed and neuromonitoring signals are confirmed to be unchanged, MAP can be returned to its original level.

When temporary clipping of parent vessels is not an option for anatomic/morphologic reasons, adenosine-induced flow arrest offers a unique method of transiently and profoundly reducing systolic blood pressure so as to facilitate clip ligation of the aneurysm.7 Other techniques to reduce aneurysm neck turgor that have been described include deep hypothermic circulatory arrest, temporary occlusion of the extracranial common carotid artery, and endovascular balloon catheter retrograde suction deflation.8 These methods, however, are logistically more difficult to carry out. Brief periods of profound hypotension can also be produced by infusions and boluses of sodium nitroprusside or esmolol, although both of these drugs are less predictable in their dose– response relationships. Adenosine has proven to be a safe, predictable agent for achieving the brief flow arrest often needed to apply a permanent clip, and can be used repeatedly. Compared with deep hypothermic circulatory arrest, adenosine offers the advantage of avoiding the coagulopathy associated with deep hypothermia, as well as the hyperglycemia and rebound hyperthermia that occur after cardiopulmonary bypass.9 Based on our observational series, in patients receiving a background anesthetic consisting of remifentanil, 0.5 minimum alveolar concentration (MAC) of volatile anesthetic, and a propofol infusion achieving a burst suppression ratio of 0.7, there is a significant linear relationship between the dose of adenosine, the duration of asystole, and the duration of profound hypotension (Fig. 13.2). An adenosine dose of 0.35 mg per kilogram of ideal body weight (preferably delivered via a central venous catheter) is the recommended starting dose to achieve approximately 45 seconds of profound systemic hypotension.10 Timing of adenosine administration, whether planned or after inadvertent intraoperative rupture of an aneurysm, must be carefully coordinated with the neurosurgeon so that adequate working time is available for the successful placement of each clip or series of clips.

Patient Positioning

Neurovascular surgical procedures can often last anywhere from 5 to 24 hours. Careful attention by the entire operative team should be paid to the positioning of the patient. Prolonged pressure or stretch of peripheral nerves (e.g., brachial plexus, ulnar nerve) may result in peripheral neuropathy. This risk may be minimized by using sufficient padding to vulnerable pressure points, adjusting all joints so that there is not extreme stretch on any neural plexus, and utilizing neurophysiologic monitors to warn of the development of peripheral nerve injury and adjusting the affected limb to correct the problem.11 Positioning may also impact the surgical field if the patient’s trunk and limbs are not adequately secured to allow sufficient manipulation or rotation of the operating table without shifting the body. Finally, ignoring the effects of a patient’s position on jugular venous drainage or the pressure on the abdomen and chest may result in inadequate cerebral venous drainage that may impede adequate brain relaxation despite aggressive therapeutic maneuvers (e.g., excessive hyperosmotic therapy or cerebrospinal fluid [CSF] drainage). In addition, excessive neck flexion or rotation may impede venous drainage from the tongue, which, in the extremes of circumstances, could result in tongue edema and even necrosis, requiring prolonged endotracheal intubation due to airway obstruction.

Brain Bulk Management

Actively managing brain bulk, even in those patients with a normal starting intracranial pressure, may reduce direct pressure exerted by retractors in the field, thereby minimizing the risk of retractor-induced brain ischemia and injury.12 Aside from acute short-term hyperventilation, hyperosmolar therapy has long been the cornerstone of brain bulk and intracranial pressure treatment. Mannitol and hypertonic saline are the osmotic agents of choice (Table 13.3). 13 ^– 15 Both agents decrease brain bulk and intracranial pressure by two different mechanisms. The initial mechanism is a decrease in blood viscosity that improves flow and increases oxygen delivery to brain tissue. This results in a compensatory vasoconstriction that reduces cerebral blood volume and therefore intracranial pressure. The delayed but major mechanism of reduced brain bulk is an osmotically mediated decrease in brain water content. Mannitol is renally excreted and produces a strong osmotic diuretic effect. Hypertonic saline, on the other hand, has a relatively small natriuretic effect, making it an attractive alternative to mannitol in certain circumstances (e.g., when cerebral perfusion pressure is difficult to maintain otherwise). Prospective, randomized, double-blind studies comparing the effects of hypertonic saline and mannitol on brain relaxation and serum electrolyte balance showed that both modalities were efficacious, though hypertonic saline may be more efficacious in achieving brain relaxation in supratentorial brain tumor patients. In addition, the mannitol group had decreased serum sodium, a greater fluid deficit, and increased plasma lactate levels compared with the hypertonic saline group.14 ^, 15 Depending on the extent of initial brain bulk, 0.25 to 1 g/kg of mannitol is usually infused intravenously over 10 to 20 minutes. Alternatively, a dose of 1 to 2 mL/kg of 3% saline can be given as an intravenous bolus, followed by an infusion of 1 to 2 mL/kg/h with a plasma sodium goal of 145 to 155 mEq/dL. If repeated doses of mannitol, or long-term infusions of hypertonic saline, are needed, plasma osmolality should be closely monitored and kept under 320 mOsm/L. In addition, care should be taken to monitor for rebound cerebral edema that may occur with the abrupt discontinuation of any infusions of a hyperosmotic agent.16

There are other effective ways of decreasing brain bulk (Table 13.4). Perhaps the simplest, and often most effective, way to manage brain bulk is to pay close attention to head and neck positioning. During fixation of the Mayfield device to the operating room table, care must be taken to avoid excessive flexion or rotation of the neck that may obstruct cerebral venous outflow. Placing the patient in 10 to 30 degrees of reverse Trendelenburg position facilitates venous outflow as well as CSF drainage and lowers intracranial pressure (ICP). However, if orthostatic hypotension occurs it should be treated with volume replacement or vasoconstrictors to maintain adequate cerebral perfusion pressure.

As mentioned above, hyperventilation-induced hypocapnia, with a goal PaCO₂ of 30 mm Hg, rapidly and effectively reduces ICP; more aggressive hyperventilation can aggravate cerebral ischemia through excessive vasoconstriction. This effect on cerebral arterial resistance is short lived because the brain compensates for CSF respiratory alkalosis by increasing bicarbonate elimination from the CSF.

Decreasing the cerebral metabolic rate (CMR) effectively reduces brain bulk by decreasing cerebral blood flow requirements. There are two methods of decreasing CMR. The administration of a bolus or infusion of a hypnotic such as thiopental or propofol is the most rapid and controllable method. Hypothermia, on the other hand, is more difficult to achieve rapidly without overshoot. Moreover, hypothermia is not only difficult to reverse due to the lack of efficient rewarming devices, but also, if the core temperature is <33.5°C, it may produce a coagulopathy and hypokalemia that not only cause surgical and hemodynamic disturbances, respectively, but also may result in delayed awakening secondary to decreased metabolic clearance of anesthetics (e.g., propofol, neuromuscular junction blocking agents). Although volatile agents decrease CMR, they are direct cerebral arterial dilators. Therefore, when other modalities have failed to provide adequate brain relaxation, their discontinuation can also be considered, and a total intravenous anesthesia technique, utilizing an opioid and 100 to 200 μg/kg/min of propofol, can be used instead.6