Neuroanesthesia and Monitoring for Cranial and Complex Spinal Surgery

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Neuroanesthesia and Monitoring for Cranial and Complex Spinal Surgery SHOBANA RAJAN, DEEPAK SHARMA

CLINICAL PEARLS • A systematic preanesthesia evaluation including optimization of coexisting diseases is critical for optimal perioperative care, preventing last-minute cancellations and reducing the risk of adverse outcomes. • The perioperative surgical home is a team-based model of care, the goals of which are to guide patients through their surgical experience, enhancing the quality of care and recovery, improving outcomes, reducing costs, and improving patient satisfaction. • The overarching goals of neuroanesthesia are to provide anesthesia and analgesia, optimize systemic and cerebral hemodynamics, provide good operating conditions, and facilitate early emergence from anesthesia. • Various anesthetic agents have unique systemic and cerebral pharmacodynamics effects and a specific pharmacokinetic profile. The choice of pharmacologic agents is determined by several factors including patient characteristics, neurologic pathology, planned surgical procedure, and intraoperative neuromonitoring. A balanced anesthetic technique incorporating potent, short-acting opioids is often used. • Airway management in neurosurgical patients is critical, particularly in those with unstable cervical spine and raised intracranial pressure. Successful airway management involves careful selection of pharmacologic agents as well as airway devices ranging from conventional direct

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euroanesthesia for cranial and complex spinal surgery involves perioperative management including preanesthetic evaluation, administration of anesthesia accounting for the neurologic presentation and intraoperative neurophysiologic monitoring, emergence and recovery from anesthesia, and postoperative recovery. Successful anesthetic management requires an understanding of neurophysiology, anesthetic neuropharmacology, and neuromonitoring in addition to the establishment of perioperative care pathways in collaboration with the surgical team. This chapter provides an overview of the perioperative and anesthetic management for neurosurgery.



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laryngoscopy to video laryngoscopes and fiberoptic bronchoscope. Intraoperative management of intracranial pressure includes osmotherapy, hyperventilation, appropriate positioning, drainage of cerebrospinal fluid, maintaining hemodynamic stability, and adequate depth of anesthesia. Despite the lack of robust evidence, pharmacologic burst suppression is often used to provide intraoperative neuroprotection in the setting of global and focal cerebral injury and in cases of cerebrovascular disease. Intraoperative neuromonitoring is commonly performed for early detection of iatrogenic neurologic injury. Electroencephalography, electrocorticography, somatosensory evoked potentials and motor evoked potentials, as well as visual and auditory evoked potentials are the most commonly used monitoring modalities. Near-infrared spectroscopy and jugular venous oximetry are used for monitoring global cerebral oxygenation, and transcranial Doppler ultrasonography is used to monitor the cerebral circulation in select neurosurgical procedures. Anesthesia for spine surgery involves care during positioning, perioperative pain management, strategies to prevent and manage excessive bleeding, prevention of postoperative visual loss, and goal-directed fluid therapy management of the airway in the case of an unstable cervical spine.

Preanesthetic Evaluation The fundamental goals of preanesthetic evaluation are to obtain pertinent patient information, preoperative optimization, risk assessment, and formulation of suitable anesthetic plan. Preanesthetic evaluation is a critical component of the perioperative surgical home model (Fig. 5.1), which incorporates, among other things, efforts to reduce unnecessary interventions that do not have the potential to benefit patients (eg, routine preoperative laboratory studies) as well as efforts to reduce cancellations and postoperative lengths of hospital stay. The preanesthesia evaluation improves perioperative care, prevents 87

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Perioperative

Patient history

Physical examination

Review of patient records

Risk assessment

Patient education and planning for anesthesia

Multidisciplinary involvement and optimization

Surgical Home

• Figure 5.1  The perioperative surgical home model.

delays/last-minute cancellations, and reduces the risk of adverse patient outcomes. It also decreases the cost of unnecessary routine medical consultations.1 In addition to the evaluation pertinent to the condition requiring neurosurgery, the preanesthesia evaluation includes eliciting a history of concurrent medical problems (such as hypertension, coronary artery disease, pulmonary disease, endocrinopathy, and renal disease). The severity, degree of control, and potential for preoperative optimization are ascertained. An assessment of the patient’s functional capacity is documented. Surgical and anesthetic history is enquired focusing on any difficulties in airway management, allergic reactions to medications (anaphylaxis, latex allergy, contrast dye allergy), postoperative nausea and vomiting, pain control, and any adverse events. Medication history is recorded. Patients on corticosteroids may need supplementation in the perioperative period. Beta-blockers and antihypertensives are usually continued in the preoperative period, although angiotensin-converting enzyme (ACE) inhibitors and anticoagulants may be stopped preoperatively. The patient’s social history, including any history of smoking as well as alcohol and illicit drug intake, is documented, given the implications for organ function, drug dosing, and the risk of adverse reactions during surgery (eg, hypertensive crises and myocardial ischemia in patients on cocaine). A family history of malignant hyperthermia and pseudocholinesterase deficiency is critical. Malignant hyperthermia is a rare complication triggered by specific anesthetic agents and could be fatal if encountered; hence avoidance of potential triggering agents is paramount. Pseudocholinesterase deficiency is associated with prolonged recovery from the neuromuscular blocking agents succinylcholine and mivacurium,2 necessitating avoidance of these muscle relaxants. The preanesthetic evaluation includes a physical examination to record vital signs (blood pressure, heart rate, respiratory rate, oxygen saturation) and body mass index (BMI). Establishing baseline blood pressure is important in neurosurgical patients to ensure optimal perioperative maintenance of cerebral and spinal perfusion. An increased BMI predicts difficulties with airway management. In addition, obesity is associated with heart disease and diabetes mellitus. Airway examination is a vital component of the physical examination from the anesthesiologist’s perspective. Inadequate management of the airway may adversely affect the neurologic outcome. Hence the patient’s airway should be assessed carefully for the ease of ventilation and tracheal intubation, in consideration with

TABLE Preanesthetic Airway Assessment 5.1  Mouth opening

Should be adequate to insert a laryngoscope safely

Mallampati classification (class I–IV)

Higher grades—difficult intubation

Neck mobility

Limited extension—poor glottic visualization

Thyromental distance

< 7 cm—indicative of anterior larynx

Neck circumference

>17 inches in men and >16 inches in women—predicts difficulty with ventilation and intubation

specific surgical needs such as hemodynamic stability and spinal immobilization. Mallampati scoring,3 thyromental distance, the presence of overbite or underbite, and neck flexion/ extension collectively provide an estimate of the risk of difficult intubation (Table 5.1). Difficult airway should be anticipated in patients with recent supratentorial craniotomy in whom the mouth opening might be significantly reduced secondary to ankylosis of the temporomandibular joint, and in patients with acromegaly or cervical spine lesions. Timely recognition of potential airway difficulty allows proper planning with accessory equipment and resources, as well as formulation of a backup plan, enhancing patient safety. Review of laboratory tests is important to rule out anemia, thrombocytopenia, renal and electrolyte abnormalities, coagulation abnormalities, and pregnancy (if applicable). Ensuring a current type and screen and antibody screen is invaluable in surgeries associated with major blood loss. According to the American Society of Anesthesiologists Task Force on preanesthesia evaluation, preoperative tests may be ordered, required, or performed selectively on the basis of clinical characteristics for purposes of guiding or optimizing perioperative management.4 For example, a preoperative resting 12-lead electrocardiogram (ECG) is reasonable for patients with known coronary heart disease, significant arrhythmia, peripheral arterial disease, cerebrovascular disease, or other forms of significant structural heart disease. Hemoglobin or hematocrit, serum glucose and electrolytes, and coagulation studies are indicated in most

CHAPTER 5  Neuroanesthesia and Monitoring for Cranial and Complex Spinal Surgery

neurosurgical patients, whereas blood levels of phenytoin may sometimes be required. Patients with dyspnea of unknown origin and patients with heart failure with worsening dyspnea or other change in clinical status may need a preoperative evaluation of left ventricular function. An important aspect of the preanesthesia evaluation is the identification of high-risk patients in order to provide better perioperative management, inform patients about expected risks, make selective referrals before surgery, order specialized preoperative investigations, initiate preoperative interventions intended to decrease perioperative risk, and arrange for appropriate levels of postoperative care.5 The American Society of Anesthesiologists (ASA) physical status classification is widely used for this purpose (Table 5.2).6 The Revised Cardiac Risk Index (RCRI) is a simple and widely used index for predicting major cardiac complications after noncardiac surgery.7 It incorporates six equally weighted components: coronary artery disease, heart failure, cerebrovascular disease, renal insufficiency, diabetes mellitus, and high-risk surgical procedures. Patient education is another key component of the preanesthesia evaluation. The ASA guidelines recommend a minimum fasting period of 2 hours for clear liquids and 6 hours for light meals in order to reduce the severity of complications related to pulmonary aspiration of gastric contents.8 It is now recognized that optimal management of the perioperative period in a nonfragmented fashion producing a continuum of care can enhance recovery, lower medical and surgical complications, and reduce cost and length of hospital stay. This is the concept of enhanced recovery and the perioperative surgical home. The perioperative surgical home is a team-based model of care the goals of which are to guide the patient through the surgical experience and enhance the quality of care, thereby enhancing recovery, improving outcomes, reducing costs, and improving patient satisfaction. Having a systematic preanesthesia evaluation is critical to this model.9

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Neurophysiology and Anesthetic Neuropharmacology The major goals in neuroanesthesia are to ensure that the patient is safely anesthetized with adequate analgesia and amnesia, effective control of cardiovascular and respiratory parameters, and maintenance of adequate perfusion to the brain and spinal cord while providing optimal conditions for the surgeons to operate. Anesthetic agents and techniques have different effects on the cerebral circulation, metabolism, and intracranial pressure (ICP) both in normal and pathologic conditions, and they have to be accounted for in successful anesthetic management. The normal brain receives 14% of the cardiac output while consuming 20% of the oxygen intake. The cerebral blood flow (CBF) is coupled to metabolic needs. The CBF remains relatively constant at approximately 50 mL/100 g/min over a wide range of cerebral perfusion pressures (CPPs), although the actual limits of autoregulation vary. For a given value of blood pressure, the CBF may be either higher or lower than that estimated by the traditional autoregulatory curve. Therefore the management of CBF should be guided by a multifactorial but integrated framework of CBF regulation, especially in patients who are at risk of cerebral ischemia. The CPP is dependent on mean arterial pressure and ICP. The latter is dependent on intracranial blood volume (CBV), brain mass, cerebrospinal fluid volume, and central venous pressure. The cerebral blood flow is profoundly influenced by the PaCO2 and, to a smaller extent, the PaO2. Within the physiologic range of 20 to 60 mm Hg, the CBF changes by 3% to 4% per mm Hg change in CO2 tension, with an accompanied decrease in CBV within seconds of changing the CO2. Thus acute hyperventilation quickly reduces CBV and ICP. However, excessive hyperventilation may cause iatrogenic ischemia. Prolonged change in systemic CO2 tension is accompanied by active transport of bicarbonate in or out of cerebrospinal fluid

TABLE American Society of Anesthesiologists Physical Status Classification System 5.2  ASA I

A normal healthy patient

Healthy, nonsmoking, minimal alcohol use.

ASA II

A patient with mild systemic disease

Examples are smoking, pregnancy, social alcohol drinking, obesity, diabetes mellitus, and hypertension (well controlled).

ASA III

A patient with severe systemic disease

Poorly controlled diabetes, hypertension, alcohol dependence, pacemaker, low ejection fraction, end stage renal disease, and so on. A neurosurgical patient usually falls into this category.

ASA IV

A patient with severe systemic disease that is a constant threat to life

Examples include recent myocardial infarction, cerebrovascular accident, coronary artery disease, ongoing cardiac ischemia or severe valve dysfunction, severe reduction of ejection fraction, sepsis, and the like.

ASA V

A moribund patient who is not expected to survive without the operation

Examples include massive trauma, intracranial bleed with mass effect, multiple organ/system dysfunction.

ASA VI

A declared brain-dead patient whose organs are being removed for donor purposes

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to restore a normal acid-base balance. Thus the effects of hyperventilation on CBF are not sustained beyond 24 hours.10 With the onset of hyperventilation, the pH of both CSF and the brain’s extracellular fluid space increases, leading to an abrupt decrease in CBF. However, due to alterations in function of the carbonic anhydrase enzyme, there is extrusion of bicarbonate from the CSF, and the pH returns to normal in 8 to 12 hours. Hence only brief duration of mild to moderate hyperventilation should be instituted selectively. Hypoxemia causes vasodilatation of the cerebral vessels and an increase in CBF, but this does not occur until the PaO2 is less than 50 mm Hg. These homeostatic mechanisms may be impaired in the neurosurgical patients. Thus cerebral metabolism is depressed in a patient with an altered level of consciousness, ICP may be elevated, flow-metabolism coupling may be lost, autoregulation may be impaired, and the blood-brain barrier may be disrupted. Except in severe injury, CO2 reactivity is usually preserved. In the anesthetized patient, the cerebral circulation is affected by multiple processes: anesthesia causing suppression of cerebral metabolic activity,11 drug- and dose-related effects of the anesthetic agents on cerebral vasculature,12,13 suppression of the sympathetic nervous activity,14 and disturbance of the systemic hemodynamics. Moreover, cardiac output could alter the cerebral circulation and CBF by its effect on the cerebrovascular resistance.15 Intravenous anesthetic agents, including thiopental and propofol, are indirect cerebral vasoconstrictors, reducing cerebral metabolism coupled with a corresponding reduction of CBF. Both autoregulation and CO2 reactivity are preserved. Ketamine is a weak noncompetitive N-methyl-D-aspartate (NMDA) antagonist that has sympathomimetic properties. Its cerebral effects are complex and are partly dependent on the action of other concurrently administered drugs. Etomidate decreases the cerebral metabolic rate,

Provide adequate depth of anesthesia and analgesia during periods of noxious stimulation (intubation, pinning, drilling of bone, etc.)

Provide adequate surgical conditions (brain relaxation, control of intracranial pressure)

Optimize cerebral and systemic physiology (cerebral blood flow and oxygenation, glycemic control etc. )

CBF, and ICP. At the same time, because of minimal cardiovascular effects, CPP is well maintained. Although changes on EEG resemble those associated with barbiturates, etomidate enhances somatosensory evoked potentials and causes less reduction of motor evoked potential amplitudes than thiopental or propofol. However, it may reduce tissue oxygen tension. Dexmedetomidine is a highly selective alpha-2 adrenoreceptor agonist that provides sedation without causing respiratory depression, does not interfere with electrophysiologic mapping except when used in higher doses, and provides hemodynamic stability. It is particularly useful for implantation of deep brain stimulators in patients with Parkinson disease and for awake craniotomies, when sophisticated neurologic testing is required. The cerebral effects of inhaled anesthetics are twofold: they are intrinsic cerebral vasodilators, but their vasodilatory actions are partly opposed by flow-metabolism coupling mediated vasoconstriction secondary to a reduction of the cerebral metabolic rate. The overall effect is unchanged flow during low-dose inhalation anesthesia but increased flow during high doses. Despite the vasodilatory potential of volatile anesthetics, they have been successfully used in neuroanesthesia without any deleterious effects, usually in concentrations less than the minimum alveolar concentration (MAC). However, when the intracranial pressure is raised sufficiently to produce a severe decrease in compliance, omitting them and using a predominantly total intravenous anesthesia (TIVA) may be prudent.

Anesthesia for Craniotomy The major anesthetic goals for craniotomy are depicted in Fig. 5.2. Neurosurgical procedures are usually done under general anesthesia with intubation and controlled ventilation (except awake craniotomies). Induction of anesthesia and tracheal

Perioperative hemodynamic control (maintain cerebral perfusion, avoidance of emergence hypertension)

Facilitate intraoperative neurophysiological monitoring (evoked potentials, electroencephalography, electrocorticography etc)

Provide intraoperative neuroprotection (e.g. burst suppression during temporary clipping)

Anesthetic goals for craniotomy

Provide timely smooth emergence avoiding coughing and straining to facilitate early neurological evaluation

Control postoperative pain, nausea and vomiting

• Figure 5.2  Anesthetic goals for craniotomy.

CHAPTER 5  Neuroanesthesia and Monitoring for Cranial and Complex Spinal Surgery

intubation are critical periods for patients with compromised intracranial compliance. The goal of the anesthetic technique should be to induce anesthesia and intubate the trachea without increasing ICP or compromising CBF and CPP. Arterial hypertension during induction increases CBV and promotes cerebral edema. Sustained hypertension can lead to marked increases in ICP, decreasing CPP and risking herniation. Excessive decreases in arterial blood pressure can be equally detrimental by compromising CPP. The most common induction technique employs propofol with modest hyperventilation to reduce ICP. A neuromuscular blocker is given to facilitate ventilation and prevent straining or coughing during intubation, both of which can abruptly increase ICP. An intravenous opioid given with propofol blunts the sympathetic response; in addition, a short-acting beta-blocker such as esmolol may be used to prevent tachycardia associated with intubation. Nondepolarizers such as vecuronium or rocuronium are used for intubation. Succinylcholine is the agent of choice for rapid sequence induction or when there are concerns about a potentially difficult airway. Anesthesia can be maintained with inhalational anesthesia, TIVA, and a combination of an opioid. Even though periods of stimulation are few, neuromuscular blockade is recommended to prevent straining, bucking, or movement while allowing motor evoked potential monitoring. Increased anesthetic requirements can be expected during the most stimulating periods: skin incision, dural opening, periosteal manipulations, including Mayfield pin placement, and closure. Intravenous anesthesia with propofol is commonly used for craniotomy because it produces dose-related decreases in CBF, the cerebral metabolic rate of oxygen (CMRO2), and ICP; has a rapid onset and offset of action; causes minimal interference with electrophysiologic monitoring; and its metabolic suppressant effect may provide neuroprotection.16 However, it can decrease the mean arterial blood pressure, and attention should be paid to maintaining CPP. Given the evidence of potential neuroprotective properties, there is resurgence of interest in the use of ketamine for neurosurgery.17 Opioids are part of the balanced anesthetic technique to provide analgesia in the preoperative period. Traditional opioids such as morphine, meperidine, and hydromorphone are in general not preferred for cranial surgery due to their longer half-life potentially interfering with timely neurologic evaluation. Short-acting agents such as fentanyl and remifentanil are more commonly used for cranial surgery. Remifentanil is a selective mu opioid receptor agonist of high potency, making it a highly capable agent to tackle the variable physiologic stressors that occur during a neurosurgical case. It is rapidly hydrolyzed by nonspecific plasma and tissue esterases: this imparts brevity of action. Its action is precise and is easily titrated. It is noncumulative and offers rapid recovery after administration ceases (attributable to rapid clearance). The context-sensitive half-life is very short (3 to 4 minutes), independent of the duration of infusion. Its unique pharmacokinetic profile makes it highly desirable in neuroanesthesia. Although it can facilitate early neurologic evaluation, its analgesic effect is evanescent and it can cause tolerance and hyperalgesia.

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Airway Management in Neuroanesthesia Careful airway management involving securing and maintaining airway patency and ensuring adequate ventilation and oxygenation is critical for neurosurgical procedures. The American Society of Anesthesiologists provides a practice advisory and a “difficult airway algorithm” that offers guidelines for the evaluation and management of a difficult airway situation. Successful airway management consists of proper preoperative assessment. Making a choice between an awake intubation and an asleep intubation often depends on the anticipated difficulty of mask ventilation. Tables 5.3 and 5.4 list factors that predict difficult mask ventilation and difficult intubation, respectively. The Mallampati score predicts the ability to have a full laryngoscopic view of the airway during intubation.3 Adequacy of neck extension is important because it enables the patient to be in the sniffing position during intubation, which helps alignment of the long axes of the mouth, the oropharynx, and larynx. An inability to assume the sniffing position is a predictor of difficult intubation. Imaging studies can provide additional information before definitive airway management is decided, depending on the urgency or emergency of the situation. Computed tomography (CT) and magnetic resonance imaging (MRI) may help to determine the nature of a possible difficult airway. Induction of anesthesia leads to decreases in functional residual capacity (FRC) attributable to the supine position, TABLE Factors Predicting Difficult Mask Ventilation 5.3  Age > 55 years Body mass index > 26 (obesity) Edentulous Presence of a beard History of snoring Airway tumors

TABLE Factors Predicting Difficult Intubation 5.4  History of difficult intubation Inability to assume sniffing position with limitation of neck extension Poor mouth opening (inter-incisor gap < 3 cm) Improper dentition with prominent incisors High arched palate High Mallampati score > 3 Thyromental distance < 6–7 cm High upper lip bite test score

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muscle paralysis, and the direct effects of the anesthetic agents. Preoxygenation is the process of allowing the patient to breathe 100% oxygen through a mask prior to the anesthetic induction in order to replace the nitrogen in the lungs with oxygen, thereby increasing the length of time before hemoglobin desaturation occurs in a patient with apnea. This lengthened apnea time provides a margin of safety while the anesthesiologist secures the airway and resumes ventilation. It is critical to avoid hypoxia and hypercarbia during airway management in neurosurgical patients. The most common technique for the induction of general anesthesia is the standard intravenous induction, which entails the administration of a rapid-acting intravenous anesthetic followed by a muscle relaxant, which improves intubating conditions by facilitating laryngoscopy, preventing both reflex laryngeal closure and coughing after intubation. Rapid sequence induction (RSI) is a variation of the standard intravenous induction commonly used when the risk for gastric regurgitation and pulmonary aspiration of gastric contents is present (eg, in patents with intracranial hypertension). After adequate preoxygenation and while cricoid pressure is applied, and the trachea is intubated without attempts to provide positive pressure ventilation by bag and mask. The goal is to achieve optimal intubating conditions rapidly so as to minimize the length of time between the loss of consciousness and securing the airway with a cuffed tracheal tube. Cricoid pressure involves the application of pressure at the cricoid ring to occlude the upper esophagus, thereby preventing the regurgitation of gastric contents into the pharynx. In situations of expected difficult mask ventilation and difficult intubation, the safest approach to airway management is to secure the airway while the patient remains awake.18 Topical application of local anesthetics on the airway is essential in this situation. Lidocaine is the most commonly used local anesthetic for awake airway management because of its rapid onset, high therapeutic index, and availability in a wide variety of preparations and concentrations.19 Other agents such as benzocaine and cocaine can also be used. Topical anesthesia targets the glossopharyngeal nerve, the superior laryngeal nerve, and the recurrent laryngeal nerve, all of which provide for sensory supply of the oropharynx and larynx. The airway is then secured using fiberoptic intubation. A variety of video laryngoscopes have now become available and have revolutionized airway management. In addition, the supraglottic airway, otherwise called the laryngeal mask airway (LMA), has also enhanced the ability to ventilate the patient. The LMA refers to a diverse family of devices that are blindly inserted into the pharynx to provide a patent conduit for ventilation, oxygenation, and delivery of anesthetic gases without the need for tracheal intubation. The LMA is a pivotal component of the ASA difficult airway algorithm. Fig. 5.3 shows a typical preparation for managing an anticipated difficult airway. Airway management is critical in cervical spine surgery to avoid injury to the cervical cord. The key in this scenario is maintaining the neck in a neutral position with minimal neck movement during endotracheal intubation. The use of video laryngoscopes is beneficial in this scenario. Studies comparing upper cervical vertebral motion during intubation using direct

• Figure 5.3  Preparation for anticipated difficult airway with fiberoptic bronchoscope; laryngeal mask airways (classic and intubating).

TABLE Strategies for Intraoperative Brain Relaxation 5.5  and Control of Intracranial Pressure 1. Maintenance of adequate depth of anesthesia and analgesia 2. Selection of appropriate anesthetic agents (intravenous anesthetics for patients with anticipated brain swelling) 3. Optimal positioning with slight head elevation and avoiding excessive neck flexion or rotation 4. Optimization of hemodynamic parameters 5. Controlled ventilation with normocarbia to moderate hypocarbia (PaCO2 30–35 mm Hg)a 6. Mannitol (osmotic diuretic) 7. Furosemide 8. Hypertonic saline 9. Cerebrospinal fluid drainage (external ventricular drainage) 10. Steroids in patients with tumors/vasogenic edemab 11. Treatment of fever/seizures 12. Burst suppression with propofol/thiopental bolus Brief periods of hypocarbia with PaCO2 < 30 mm Hg should be used only in emergent conditions or when other intracranial pressure reduction maneuvers have failed. b Steroids should not be administered in patients with traumatic brain injury. a

laryngoscopy, LMA, and fiberoptic intubation show that the fiberoptic produced the least motion in the upper cervical spine.20,21 Not surprisingly, fiberoptic intubation is often the preferred method for airway management during cervical spine surgeries.

Osmotherapy and Diuretics The anesthetic strategies for providing intraoperative brain relaxation and control of ICP are listed in Table 5.5. Mannitol is the most commonly used osmotic diuretic intraoperatively because of its effectiveness in rapid reduction of brain volume.

CHAPTER 5  Neuroanesthesia and Monitoring for Cranial and Complex Spinal Surgery

The doses are usually between 0.25 g/kg and 1 g/kg. Mannitol should be administered by infusion over 10 to 15 minutes and may need to be repeated. If given rapidly, it can increase circulating volume, which although temporary can be dangerous in a patient with poor cardiac function. It can also cause electrolyte imbalance and volume depletion. In the critical care environment, the use of hypertonic saline (HTS) in place of mannitol is increasing.22 HTS does not cause diuresis and volume depletion and hence may be useful in situations of hypovolemia. A hypertonic saline bolus may be administered in concentrations ranging from 3% to 23.4% with goal of serum sodium between 140 and 150 meq/L. Concentrations > 2% must be given through a central venous catheter. In addition, there are anecdotal reports of HTS being effective in patients who were refractory to mannitol.23 Loop diuretic (usually furosemide) is sometimes combined with an osmotic diuretic, the rationale being that mannitol establishes an osmotic gradient that draws fluid out of brain parenchyma and furosemide by hastening the excretion of water from the intravascular space, maintaining the gradient. Neurons and glia have homeostatic mechanisms to ensure the regulation of cell volume. Although they shrink in response to the increased osmolarity produced by mannitol, they recover their volume rapidly as a consequence of the accumulation of idiogenic osmoles, which minimizes the gradient between the internal and external environments. One of those idiogenic osmoles is chloride. Loop diuretics inhibit the chloride channel through which this ion must pass and thereby retard the normal volume-restoring mechanism.

Burst Suppression Pharmacologic burst suppression has been an area of tremendous interest due to its attractive potential to provide neuroprotection in the setting of acute cerebral injury. It has been studied in the setting of both global and focal cerebral injury. Anesthetic agents such as barbiturates, propofol, etomidate, midazolam, and inhalation agents can produce a large reduction (approximately 50%) in the cerebral metabolic rate of oxygen, which could help to protect the brain in situations of CBF compromise. Anesthetic burst suppression has not been found to be of clear benefit in comatose survivors of cardiac arrest24 and cerebral aneurysm surgery.25 There is insufficient evidence in the setting of traumatic brain injury to determine benefit or harm.26 Current indications for pharmacologic burst suppression based on low-level evidence include refractory status epilepticus,27 refractory intracranial hypertension (such as in traumatic brain injury),28 and intraoperative neuroprotection during cerebrovascular (such as carotid endarterectomy) surgery.29 Burst suppression is titrated to electroencephalographic (EEG) monitoring as is often quantified as a burst suppression ratio although an optimal burst suppression ratio is unknown. Maintenance of mean arterial pressure is important during periods of burst suppression, which can result in severe hypotension due to the vasodilatory potential of anesthetics. To ensure collateral flow and perfusion, it is important to keep the systemic pressures elevated with the help of

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vasopressors and to limit the duration of episodes of temporary occlusion. Burst suppression can often delay the emergence at the end of surgery, and hence reducing its duration to the minimum essential is desirable.

Hemodynamic Management in Cerebrovascular Diseases Aneurysmal Subarachnoid Hemorrhage The two major complications contributing to significant morbidity and mortality after subarachnoid hemorrhage (SAH) are rebleeding and vasospasm. Most experts recommend a systolic blood pressure < 140 mm Hg in a patient with no history of hypertension. Systolic blood pressure > 150 mm Hg has been associated with aneurysmal rerupture; at the same time, too low a blood pressure can lead to cerebral ischemia. The incidence of aneurysm rupture during the induction of anesthesia, although rare, is usually precipitated by a sudden rise in blood pressure during tracheal intubation. Therefore the goal during the induction of anesthesia for aneurysm surgery is to reduce the risk of aneurysm rupture by avoiding any increase in the transmural pressure. Prophylaxis for the normal hypertensive response to intubation should be instituted before tracheal intubation with pharmacologic agents such as intravenous lidocaine and short-acting, titratable medications such as esmolol or nicardipine to reduce blood pressure. During dissection of the aneurysm, the anesthetic goal is to maintain normotension and avoid hypertension. Most surgeons use temporary occlusion of the major feeding artery.30 The potential risks of temporary occlusion include focal cerebral ischemia and subsequent infarction as well as damage to the feeding artery from the occlusion. Five to 7 minutes of occlusion with prompt reperfusion is usually well tolerated, but this time period is generally insufficient for a giant aneurysmal sac. Hence in order to extend the duration of temporary clipping many institutions use burst suppression. Mild to moderate hypothermia has also been used to extend the duration of tolerable occlusion, although it was not found to be efficacious and hence is not favored in clinical practice.25

Adenosine-Induced Cardiac Standstill Temporary clipping may not be suitable in situations when occlusion is not possible due to the location of the aneurysm (eg, paraclinoid internal carotid or basilar artery), its size (eg, a giant aneurysm interferes with the visualization of the proximal artery), or when atherosclerosis is severe in the proximal artery. In such situations, transient cardiac standstill with adenosine is an option for decompression of the aneurysm, which aids in optimally positioning the permanent clip.31 It is also useful in the event of inadvertent intraoperative rupture of the aneurysm, where it helps to maintain a clear surgical field. Adenosine induces high-degree atrioventricular block, decreasing the heart rate within seconds followed by brief asystole. The duration of adenosine-induced asystole is dose dependent but can vary considerably.32 Decompression of the aneurysm

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develops immediately with asystole and is maintained during the periods of profound-moderate hypotension before recovery of the blood pressure. Burst suppression is usually induced before causing cardiac standstill to reduce the cerebral metabolic rate of oxygen consumption during the period of asystole and hypotension. Adenosine in doses of 0.29 to 0.44 mg/kg results in about 57 (range 26–105) seconds of moderate hypotension.32 Adenosine is not suitable for patients with reactive airways disease, cardiac conduction diseases, and coronary artery disease. Cardiac arrhythmias such as transient atrial fibrillation, ventricular tachycardia, and atrial flutter may occur during cardiac rhythm recovery. Occasionally, ST segment depression may occur. With experienced providers, adenosineinduced transient asystole is an effective and safe-to-facilitate aneurysm clipping.

Arteriovenous Malformations and Hemodynamics Arteriovenous malformations (AVMs) in the brain have unique cerebral circulatory changes. There is rapid and a greater bulk of blood flow through the AVM, resulting in cerebral arterial hypotension along the path of the shunt. Patients with AVMs have a progressive decrease in arterial pressure that proceeds from the circle of Willis to the AVM nidus.33 Circulatory beds parallel with the shunt system will be perfused at lower than normal pressures even if flow remains relatively normal, leading to a leftward shift of the cerebral autoregulation curve. This phenomenon may be explained by adaptive autoregulatory displacement.34 The intraoperative appearance of diffuse bleeding from the operative site or brain swelling and the postoperative occurrence of hemorrhage or swelling have been attributed to a normal perfusion pressure breakthrough (NPPB) or “hyperemic” complications. NPPB is attributed to cerebral hyperemia due to the repressurization of previously hypotensive regions after surgery favored by uncontrolled systemic blood pressure. Hence induced hypotension may be useful during AVM resections, particularly the large AVMs that have a deep arterial supply. Bleeding from the deep feeding vessels may be difficult to control, and decreasing the arterial pressure facilitates surgical hemostasis and may prevent normal perfusion pressure breakthrough. Importantly, subnormal blood pressure (below the preoperative baseline) needs to be maintained following the resection of large AVMs.

Hypothermia For almost a century, there has been interest in using hypothermia as a potential neuroprotective measure in patients suffering from severe intracranial disease. Therapeutic hypothermia, or targeted temperature management as it is currently called, aims to attenuate the cascade of secondary injury mechanism. Hypothermia is a nonpharmacologic method of reducing the CMRO2, different from barbiturates in that it reduces not only the active but also the basal metabolism of the neuronal cells. This protective effect is greater than would be expected from metabolic suppression alone and may be related

to a decrease in excitatory neurotransmitter release from ischemic cells.35 There is good evidence favoring therapeutic hypothermia following the return of circulation after cardiac arrest.36,37 However, there appears to be no benefit to intraoperative hypothermia during intracranial aneurysm surgery.38 In a large, prospective, international, multicenter, and blinded study, 1001 patients presenting with aneurysmal subarachnoid hemorrhage in good clinical grade (a World Federation of Neurological Surgeons [WFNS] score of I, II, or III) were randomized to either the intraoperative hypothermia (target temperature 33°C, using surface cooling techniques) or the normothermia (target temperature 36.5°C) group during aneurysm surgery. Outcome was assessed at 90 days postoperatively, primarily using the Glasgow Outcome Score. No significant differences in outcome measures were found between the groups. Furthermore, there was a suggestion that postoperative bacteremia may be more common in the hypothermic group, even though there was no difference in pneumonia, meningitis, or wound infection rate. Hypothermia has also not been found to be efficacious in other neurologic conditions including traumatic brain injury.39 Moreover, the adverse effects of hypothermia, such as stress-induced decreases in oxygenation of hypoxic areas, coagulopathies, pneumonia, and rebound increase in ICP upon rewarming, may counteract any potential neuroprotective effects. Whereas the benefits of hypothermia remain to be established, hyperthermia is clearly deleterious for the brain and must be avoided.

Glucose Management Perioperative glucose control is an important and yet controversial aspect of neurosurgery. Hyperglycemia can cause secondary brain injury, leading to increased glycolytic rates evidenced by an increased lactate/pyruvate ratio, resulting in metabolic acidosis within brain parenchyma, overproduction of reactive oxygen species, and neuronal cell death.40–42 Although extremes of glucose levels should be avoided, there are few data to support an optimal blood glucose level or the specific use of intensive insulin therapy for euglycemia maintenance in the perioperative management of neurosurgical patients. Intensive insulin therapy also found a higher incidence of hypoglycemia.43–45 Hence tight glucose control with intensive insulin therapy remains controversial. There are a number of reasons why patients could be hyperglycemic in the neurosurgical population. The stress of surgery activates a neuroendocrine response that antagonizes the action of insulin and predisposes to ketoacidosis.46,47 Stress also induces the development of insulin resistance, generated by proinflammatory cytokines.48,49 Hyperglycemia can be caused iatrogenically by dexamethasone, which is commonly used in these procedures. The brain is very vulnerable to extreme blood glucose level variations. The American Diabetes Association and the American Association of Clinical Endocrinologists,50 based on the available evidence, set an upper limit at 180 mg/dL (10 mmol/L), at which insulin therapy should be started. This would also propose to maintain blood glucose levels between 140 and 180  mg/dL (7.8–10.0  mmol/L) in critically ill patients

CHAPTER 5  Neuroanesthesia and Monitoring for Cranial and Complex Spinal Surgery

and in the perioperative period. Essentially, although hyperglycemia has consistently been shown to be associated with adverse outcomes, the benefits of intensive insulin therapy remain unclear. In the perioperative period, glucose should be monitored regularly and managed according to institutional protocols using insulin infusion.

Intraoperative Neuromonitoring Perioperative neuromonitoring is important to guide not only the surgical technique but also anesthetic interventions to optimize cerebral physiology, thereby avoiding complications and potentially improving neurologic outcomes. Clinical neurologic examination with an awake, cooperative patient is often considered the gold standard of neuromonitoring. The asleepawake-asleep technique has been widely described for craniotomy for resection of seizure focus and intracranial space occupying lesions. The technique requires the patient to be awake and cooperative in order to identify the proximity of the intracranial lesion to eloquent areas of the brain such as the speech area, thus allowing the surgeon to safely perform the resection without resulting neurologic deficits. This typically involves producing a loss of consciousness in the beginning followed by maintenance of general anesthesia with or without an artificial airway (laryngeal mask airway or oropharyngeal/nasal airway) to facilitate skull block and craniotomy. After surgical exposure, the patient is smoothly awakened to participate in motor or language mapping, following which the patient may be anesthetized for resection of the intracranial lesion and closure. A variety of anesthetic agents including propofol, dexmedetomidine, and remifentanil can be successfully used for awake craniotomy.51 Awake intraoperative neurologic testing is often used during carotid endarterectomy to detect cerebral ischemia when the carotid artery is clamped.

Electroencephalography and Electrocorticography Electroencephalography (EEG) can be measured from electrodes placed over the scalp, according to the ten-twenty International System of Electrode Placement. Because the EEG appearance of ischemia and profound metabolic suppression are similar, the clinical context has to be taken into consideration. The EEG is routinely used to monitor burst suppression during cerebrovascular surgery. Intraoperative EEG monitoring is also useful to diagnose nonconvulsive seizures. Electrocorticography (ECoG) provides electrical brain signals with a high signal-to-noise ratio, less susceptibility to artifacts than EEG, and a high spatial and temporal resolution. Intraoperative ECoG is performed by the placement of a special electrode array using strips, a grid, or depth electrodes directly on the surface or within the substance of the brain. It is used not only to guide the localization of the seizure focus, but also to assess the completeness of resection of the seizure focus. The ECoG pattern depends on multiple factors such as the locations of electrodes, preoperative medications, and the anesthetic agents.

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The sharp epileptiform potentials are characteristic of epilepsy. Spontaneous interictal epileptiform activities (IEAs) are the EEG recordings obtained between clinical seizure episodes, characterized as spikes, sharp waves, or any combination thereof, and have a high positive predictive value for the diagnosis of epilepsy.52 Because the ECoG recordings are affected by anesthetics, the anesthetic agents have to be selected carefully. Maintaining a stable low anesthetic depth is important during intraoperative ECoG. Sedative doses of propofol and dexmedetomidine have minimal effect on spontaneous IEAs, making them suitable for intraoperative ECoG.53 Occasionally, there may be no spontaneous interictal discharges during the intraoperative ECoG and interventions to facilitate epileptiform activity may be needed. Alfentanil in 20- to 100-µg/kg doses reliably produces spike activation, whereas the effects of methohexital may be variable.54

Evoked Potentials Evoked potentials monitor the integrity of the central nervous system from the point of stimulus application along the neuronal pathway to the response that they elicit. They consist of primarily somatosensory evoked potentials (SEPs), motor evoked potentials (MEPs), brain auditory evoked responses (BAERs), and visual evoked potentials (VEPs). Fig. 5.4 (somatosensory evoked potentials, median nerve upper extremities) and Fig. 5.5 (motor evoked potentials, upper extremity) demonstrate a typical SEP and MEP waveform, respectively, from the upper extremity. A comparison between SEPs and MEPs is listed in Table 5.6. For SEP monitoring, a mixed motor and sensory nerve such as the median or posterior tibial nerve is electrically stimulated at the wrist or ankle, respectively, with just enough energy (10–50 mA) to depolarize both sensory and motor fibers. Depolarization of the motor fibers elicits a twitch from the innervated muscle and indicates satisfactory stimulation of the nerve. In the sensory fibers the wave of depolarization ascends along the nerve and into the dorsal root of the spinal cord to then travel rostral in the dorsal columns of the spinal cord, decussating in the medulla. To this point the transmission is fairly uninterrupted, but between the thalamus and primary sensory cortex there are a number of synapses. Because there are a number of synapses along the SEP pathway, the waveform is susceptible to the effects of anesthetic agents and physiologic factors such as hypotension and hypothermia. SEP monitoring is employed when the structures generating the signal are either directly or indirectly at risk due to injury or interruption in blood supply. The brainstem and thalamic components are vulnerable to vascular injury of the basilar artery and its perforators, whereas the early cortical waveform is particularly vulnerable to ischemia in the middle cerebral artery territory when the upper limb is stimulated and the anterior cerebral artery when the lower limb is stimulated. Cranial nerves may also be stimulated in order to elicit cortical responses. Most commonly the auditory nerve maybe stimulated with clicks delivered by earpieces placed in the auditory canal and the response measured over the corresponding auditory cortex. The brainstem component of the

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Avg 0/200

Avg 0/200

N20 +

N20 +

C4-C3 - (5)

C3-C4 - (5) + P25

+ P25 C4-Fz - (5) C3-Fz - (5)

N10 +

Fz-Mas - (5) + P14

+ N10 + P14

Fz-Mas - (5)

EP - (5) EP - (5)

5 ms/Div

5 ms/Div

• Figure 5.4  Somatosensory evoked potentials median nerve upper extremities.

Delt+ 09:10:47 - RDelt

+ Delt+

Trc+

09:10:47 - Rtn

+ Trc+ ECR+ Therm+ + ECR+

09:10:47 - REcr

09:10:47 - RTh

+ Therm+

EHL+

09:10:47 - REHL + EHL+ Ah+ 09:10:47 - RAh + Ah+

10 ms/Div

• Figure 5.5  Motor evoked potentials upper extremity.

auditory evoked response is particularly robust to the effects of anesthetic drugs and is employed during surgery for acoustic neuroma and other cerebellar pontine angle tumors to monitor the integrity of cranial nerve VIII. Visual evoked potential monitoring is technically more challenging and is not widely employed in the operating room. MEPs are typically recorded from needle electrodes placed in distal and proximal muscle groups of the upper and lower limbs and measure a compound action potential in response to electrical stimulus applied by needle electrodes placed into the scalp over the motor cortex. The signal is then carried along the cortical spinal or pyramidal tract through the internal capsule and cerebellar peduncles, decussates in the brainstem, and descends in the spinal cord synapsing with the anterior horn cell of the peripheral nerve. The MEP is particularly vulnerable to the effects of anesthetic agents at the level of the motor cortex and the anterior horn cell depolarization is particularly sensitive to the effects of inhalational anesthetic agents. MEPs are often employed during neurovascular surgery. Both SEPs and MEPs can be affected by physiologic and pharmacologic variables, and it is important that the milieu and drug concentrations be kept as constant as possible. In general, factors that interrupt the transmission of signals such as ischemia, injury, or the depressant effects of drugs tend to increase latency, decrease the amplitude of SEPs, and decrease the amplitude of MEPs. Changes can be graded from diminished to absent depending on the severity of the interruption

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TABLE A Comparison of Somatosensory and Motor Evoked Potentials 5.6 

Somatosensory Evoked Potentials (SEPs)

Motor Evoked Potentials (MEPs)

Pathway

Stimulus applied peripherally, response ascends through the CNS and recorded from electrodes placed over the somatosensory cortex.

Stimulus applied over the motor cortex and response descends through the CNS and recorded usually from muscle groups in the upper and lower limbs.

Technical Aspects

Peripheral nerve repeatedly stimulated with low-voltage stimulus and SEP waveform elicited from the background EEG by the process of signal averaging.

Most commonly, large voltage stimulus is applied over the scalp and response obtained from needle electrodes inserted into muscles. Stimulus applied as a short burst of usually 2–6 stimuli over a few seconds.

Safety Concerns

Can be run continuously

Usually cause the whole body to jolt. Timing of stimulus must be in conjunction with surgery. A bite block needs to be used to avoid injury to the tongue. Use with caution in patients with history of seizures and who are very frail.

Anesthetic Agents

Volatile anesthetics and propofol decrease the amplitude and increase latency of the waveform. Opioids have little effect. Ketamine and etomidate potentiate the signal. Dexmedetomidine has a dose-related suppressant effect. Nitrous oxide decreases amplitude. Lidocaine has little effect.

Similar to SEPs but the effect of volatile anesthetics on the amplitude of the MEP is greater than that of propofol. Desflurane has least effect of the volatile anesthetics on MEP amplitude. Nitrous oxide has a profound effect on MEP amplitude.

Muscle Relaxants

Can be used. Reduce electrical noise and improve quality of signal.

Most centers prefer not to use as they attenuate the muscle response. Can be used carefully, if train of fourmuscle response is monitored and kept constant.

Utility of Modality

Cortical response from lower limb is particularly sensitive to ischemia in territory of the anterior cerebral artery, and the response from the upper limb falls in the distribution of the middle cerebral artery.

The motor fibers are tightly bundled as they pass through the internal capsule and are particularly useful in clipping of skull base aneurysms that may involve perforators supplying this region.

and may recover depending on the etiology and duration. Both SEPs and MEPs exhibit laterality, but global factors such as drug concentration and physiologic factors will affect SEPs and MEPs bilaterally. The surgical process will often have a more unilateral effect on evoked responses and possibly affect one modality more than another. Factors such as hypotension, hypoxia, and low hematocrit that reduce perfusion and oxygen delivery will in general reduce the amplitude and increase latency of SEPs as well as decrease the amplitude of MEPs.55 Hypothermia also has a negative effect on signals.55 General anesthetic agents have a tendency to suppress the amplitude and increase the latency of SEPs and the amplitude of MEPs. Propofol has less effect on the anterior horn cell synapse of the MEP pathway and may be recommended over inhalational agents for monitoring MEPs.56 Although the MEPs can be elicited with inhalational agents, it is important to limit their alveolar concentrations to around 0.5 at minimum. This is often achieved with the concurrent use of opioid infusions, in particular remifentanil, which has little effect on MEPs. Of the commonly used inhalational agents, desflurane has the least effect on MEPs.57 The intravenous agents etomidate and ketamine have a potentiating effect (increased amplitudes) on MEPs and SEPs58 Dexmedetomidine has little effect on MEPs and SEPs at lower doses, but at higher doses it suppresses both signals.59 Neuromuscular blocking agents cause a graded loss

of amplitude on the MEP proportional to the degree of block and are therefore generally avoided with MEP monitoring; however, if the degree of neuromuscular block is closely monitored, it is possible to attenuate the movement associated with the muscular response and facilitate a more continuous use of the modality.60 If SEPs are to be used without concurrent MEPs, then the use of neuromuscular blockade actually potentiates the signal by removing electromyogram artifact.61

Intracranial Pressure and Cerebral Perfusion Pressure Elevated ICP may occur in patients with intracranial pathology such as severe traumatic brain injury, subarachnoid hemorrhage, intracranial tumors, and cerebral edema. Obviously, prompt recognition and treatment of elevated ICP is important. The ICP can be measured using an intraventricular catheter (external ventricular drain), fiberoptic monitor implanted into the parenchyma of the brain, or subdural/ epidural bolt. The intraventricular catheter provides the most accurate monitoring of ICP; it also allows for therapeutic CSF drainage to treat raised ICP. The management of ICP has the potential to influence outcome, particularly when care is targeted, individualized, and supplemented with data from other monitors.

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Jugular Venous Oximetry Jugular venous oximetry allows monitoring of cerebral oxygenation to detect intraoperative cerebral desaturation and guide anesthetic interventions such as optimizing hyperventilation therapy and management of perfusion pressure, fluids, and oxygenation to optimize the cerebral physiology.62–64 Although the jugular venous blood is derived from both cerebral hemispheres, it is recommended that a jugular bulb catheter be placed in the internal jugular vein on the side of dominant cerebral venous drainage, although it is often argued that in the presence of a focal brain injury, the catheter should be placed on the side ipsilateral to the brain injury. The cerebral venous dominance can be easily determined by examining the venous caliber on cerebral angiogram (Fig. 5.6), by computerized tomographic assessment of jugular foramen size, or by ultrasonographic comparison of the size of the internal jugular veins. Potential complications of jugular oximetry include inadvertent carotid artery puncture, pneumothorax, nerve injury, infection, and thrombosis. However, the cannulation is safe at the hands of experience providers. Normal jugular venous oxygen saturation (SjvO2) ranges from 55% to 75% with values at either extreme reflecting cerebral ischemia or hyperemia. SjvO2 ≤ 55% has been shown to be associated with poor neurologic outcome in children with traumatic brain injury (TBI).65 Jugular venous oximetry in adults during intracranial surgery can detect critical intraoperative cerebral desaturation that would otherwise have been untreated66 and guides determination of the minimum blood pressure that should be maintained to avoid global cerebral hypoperfusion during intracranial aneurysm surgery.67 Monitoring SjvO2 is helpful

RICA

in titrating hyperventilation to accomplish brain relaxation by cerebral vasoconstriction within safe limits.68 A low SjvO2 is also a transfusion trigger in the setting of low hematocrit with optimal hemodynamic and ventilator parameters.

Near-Infrared Spectroscopy Near-infrared spectroscopy (NIRS) is increasingly being used to measure regional cerebral tissue oxygen saturation (rSO2) perioperatively, largely due to the ease with which NIRS sensors can be placed on the forehead, the continuous availability of cerebral oxygenation data, and the ease of interpretation of rSO2 values coupled with gradually accumulating data supporting the utility of cerebral oximetry in various clinical settings. Normal rSO2 ranges from 60% to 75%. Changes in rSO2 may be influenced by changes in various factors including cardiac output, blood pressure, partial pressure of CO2, arterial pH, inspired oxygen concentration, temperature, local/regional blood flow, and hemoglobin concentration, and hence rSO2 monitoring may guide therapeutic interventions to optimize these parameters. The application of NIRS for monitoring cerebral oxygenation during carotid endarterectomy, specifically to guide the need for shunting during carotid cross clamping, is well accepted.

Transcranial Doppler Ultrasonography Transcranial Doppler (TCD) ultrasonography is a noninvasive, nonradioactive, and portable technique that provides continuous real-time information regarding cerebral circulation using a range-gated, pulsed-Doppler ultrasound. The cerebral blood flow velocity (CBFV) can be increased due to hyperdynamic circulation, hypercarbia, hyperemia, cerebral vasospasm, arterial stenosis, volatile anesthetics and arteriovenous malformation. Conversely, the CBFV can be decreased due to hypotension (below autoregulatory limits), hypocarbia, hypothermia, intracranial hypertension, and intravenous anesthetics. TCD ultrasonography can be used to assess cerebral autoregulation. Table 5.7 lists the perioperative applications of TCD ultrasonography.

Anesthetic Considerations for Spine Surgery In addition to possible spinal instability and neurologic deficits, the patients undergoing spine surgery often have chronic pain and could have multiple comorbidities, all of which put them at higher risk for postoperative complications and prolonged hospital stay. The major anesthetic concerns for spine surgery are depicted in Fig. 5.7. Often, spine surgeries are performed in the prone position. The considerations related to prone positioning are described in Table 5.8.

Intraoperative Blood Loss • Figure 5.6  Cerebral angiogram showing left-sided dominant cerebral venous drainage.

Patients undergoing major spinal fusion surgery are at risk of excessive blood loss requiring blood transfusion and exposure to its related complications such as immunologic reactions,

CHAPTER 5  Neuroanesthesia and Monitoring for Cranial and Complex Spinal Surgery

transmission of infections, or transfusion-related acute lung injury. Strategies to minimize these risks include increasing the preoperative red blood cell mass and reducing the intraoperative blood loss. Preoperative red blood cell mass can be optimized using erythropoietin, intravenous iron, vitamin B12, and folic acid. Preoperative autologous donation,69 intraoperative cell salvage, tranexamic acid,70 point-of-care coagulation testing, and avoidance of hypothermia are effective in reducing the necessity for blood transfusions. In spine surgery,71 the prophylactic administration of high-dose tranexamic acid (1 g, then 100 mg/h until skin closure) has been shown to decrease blood loss and the need for blood transfusions significantly.

TABLE Perioperative Applications of Transcranial 5.7  Doppler Ultrasonography Detection of intracranial vascular stenosis/cerebral spasm Detection of cerebral hyperemia Following intracranial arteriovenous malformation resection/embolization Following carotid endarterectomy Monitoring for adequacy of cerebral blood flow Extracranial arterial stenosis/occlusion (eg, neck trauma) Following extracranial-intracranial bypass surgery Carotid endarterectomy (to assess the need for shunt during carotid clamping) Head-injured patients undergoing extracranial surgery Sitting position surgery Diagnosis of right-to-left cardiac shunts (“bubble test”) Emboli monitoring Stroke Carotid endarterectomy Assessment of cerebral autoregulation Assessment of cerebrovascular reactivity to carbon dioxide

Patients treated with aspirin and clopidogrel could also benefit from point-of-care testing conducted to assess the individual efficacy of desmopressin treatment.72 Patients scheduled for elective surgery are increasingly treated with new oral anticoagulants such as direct thrombin (dabigatran) and factor Xa inhibitors (rivaroxaban, apixaban, and edoxaban). Patients treated with these drugs should only be operated on after

TABLE Prone Position–Related Concerns 5.8  Securing the endotracheal tube and intravenous and arterial lines during positioning

Disconnections or dislodgment can lead to loss of airway or vascular access

Avoidance of pressure on eyes

To avoid postoperative visual complications

Positioning of arm boards

Important to prevent stretch injuries to brachial plexus

Neutral neck position

To prevent cervical cord injury due to ischemia

Proper padding of bony prominences

To avoid excessive pressure leading to nerve palsies

Close hemodynamic monitoring

Prone positioning can cause hemodynamic fluctuations

The abdomen should hang free

Increased vena-caval pressure can lead to a reduction in spinal cord blood flow and contribute to excessive bleeding

Higher doses of radiation may be required for tissue penetration

Operative personnel are exposed to more radiation

Facilitate intraoperative evoked potential monitoring

Maintenance of spinal cord perfusion

Strategies to prevent postoperative visual loss

Providing early emergence for neurologic evaluation

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Anesthetic goals for spine surgery

Minimizing blood loss and blood transfusion

Prevention and management of postoperative pain

• Figure 5.7  Major anesthetic concerns for spine surgery.

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appropriately withholding them. High-dose prothrombin complex concentrate (PCC) is efficacious in reversing the anti-Xa effect of rivaroxaban, apixaban, and edoxaban.73

Postoperative Visual Loss Perioperative visual loss (POVL) is an uncommon but devastating complication related to spinal surgery. The reported incidence of POVL after spine surgery ranges from 0.03% to 0.2%.74–76 The common mechanism of visual loss is thought to be compression of the globe leading to increases in intraocular pressure compromising flow to the central retinal artery. Hence positioning of the head and neck with frequent checking of the eyes is important. Another proposed mechanism is posterior ischemic optic neuropathy (PION). It usually presents as painless visual loss after waking up from anesthesia. It is also associated with prolonged periods of increased venous pressure in the head as occurs in the prone position in spine surgery. The risk factors for ischemic optic neuropathy associated with spine surgery include male gender, obesity, Wilson frame use, longer operative times, greater blood loss, and a lower colloid-to-crystalloid ratio in the nonblood fluid administration.77 Numerous factors have been proposed that contribute to the development of POVL including anemia, emboli, hypotension, globe compression, prone positioning, volume or type of fluid administered, and preexisting diseases.78 The American Society of Anesthesiologists practice advisory recommends considering informing about this risk to patients in whom prolonged procedures, substantial blood loss, or both are anticipated. Significant physiologic and hemodynamic perturbations should be avoided as much as possible, and colloids should be added to the crystalloid regimen as part of intraoperative fluid therapy.79

Pain Management Perioperative pain management is a significant challenge following major spine surgery. Many pathways contribute to perioperative pain, including nociceptive, inflammatory, and neuropathic mechanisms. Opioid analgesics are often the firstline agents in the management of postoperative pain. However, many patients are chronically on opioids prior to surgery and hence may be tolerant to the opioids. These patients are likely to have an exacerbation of pain in the postoperative period requiring two to three times higher than the usual dosage due to peripheral and central sensitization contributing to both hyperalgesia and tolerance.80,81 The increased dosage can lead to side effects such as respiratory depression, cardiac complications, ileus, urinary retention, prolonged hospital stay, and decreased patient satisfaction. Multimodal pain management has the potential to decrease postoperative pain while reducing the total opioid consumption.82,83 Multimodal approaches to pain management have gained favor with the goal of targeting a number of different pain signaling pathways to reduce patient pain while minimizing side effects. The types of agents used can be chosen from any number of permutations and include nonsteroidal antiinflammatory drugs (NSAID), opioids,

muscle relaxants, anticonvulsants, and acetaminophen. There is grade B evidence that the addition of NSAIDs (eg, celecoxib) and grade A evidence that acetaminophen and gabapentinoids help with postoperative pain when used as multimodal analgesia.84,85 Gabapentin and pregabalin are second-generation anticonvulsants typically used for the treatment of chronic neuropathic pain. They work by binding the a2-d subunit of N-type voltage-gated calcium channels, thereby inhibiting the release of neurotransmitters and reducing neuronal excitability. Additional infusions of ketamine or lidocaine are increasingly being used in the intraoperative period preemptively for their effectiveness in reducing postoperative opioid consumption and enhancing recovery. Use of low-dose racemic ketamine has been shown to reduce acute postoperative analgesic consumption and pain intensity in opiate-naïve86 and opioiddependent87,88 patients undergoing a variety of surgical procedures. The opiate-sparing effect of ketamine is greatest during the 24 to 48 hours following surgery. It is thought that the efficacy of ketamine in this patient subset is due to a complex mechanism of action involving not only NMDA and opiate receptors but also the balance between excitatory and inhibitory neurotransmitters. The antiinflammatory effects of IV lidocaine are mediated by inhibition of N-methyl-D-aspartate receptors89,90 and leukocyte priming.91 Lidocaine stimulates secretion of the antiinflammatory cytokine interleukin-1 receptor antagonist92 and has been shown to reduce pain, postoperative nausea and vomiting, and major complications.93

Enhanced Recovery After Surgery Pathways It is now recognized that optimal management of the perioperative period in a nonfragmented fashion producing a continuum of care can enhance recovery, lower medical and surgical complications and reduce cost and length of hospital stay. This is the concept of enhanced recovery and perioperative surgical home. Preadmission counseling, nutrition, optimal multimodal analgesia, optimal fluid therapy, perioperative glycemic control, prevention of hypothermia, and prevention of postoperative nausea and vomiting are all key components in the enhanced recovery pathways. The concept of enhanced recovery after surgery (ERAS), also called fast-track, accelerated, or rapid recovery was first introduced by Henrik Kehlet.94 The enhanced recovery after surgery pathway is designed to speed recovery by improving quality of perioperative care not by discovering new knowledge but rather by integrating what is already known into practice. The central elements of the ERAS pathway address the key factors, such as patient education, improved preoperative nutrition, decreased duration of fasting, carbohydrate loading preoperatively, multimodal pain management, appropriate fluid therapy, using short-acting anesthetic agents, strategies to minimize blood loss, maintenance of body temperature, prevention of postoperative nausea and vomiting, early ambulation, physical therapy, and rehabilitation. Although there is strong evidence that the ERAS pathways are beneficial in colorectal surgery,95 there is still paucity of evidence for their benefit in spine surgery.

CHAPTER 5  Neuroanesthesia and Monitoring for Cranial and Complex Spinal Surgery

Fluid Management in Neurosurgical Patients During major surgery, the goals of fluid therapy are to maintain cellular homeostasis with adequate tissue perfusion, cellular integrity, and electrolyte balance. Intraoperative fluid management of neurosurgical patients presents a unique challenge for the anesthesiologist. Neurosurgical patients can be hypovolemic due to the administration of potent diuretics, associated diabetes insipidus, cerebral salt wasting, or blood loss in a situation of traumatic brain injury. In addition, there is a concern to keep the cerebral water content low to avoid cerebral edema and raised intracranial pressure. There may be associated electrolyte imbalances due to the use of osmotic agents and diuretics, making this a complex situation. Important determinants of fluid movement across the blood-brain barrier, such as osmolarity and oncotic pressure, should be considered while selecting the type of fluid. Control of cerebral hemodynamics begins with control of systemic arterial pressure, which in turn is predicated on adequate cardiac preload. The blood-brain barrier is a highly selective permeability barrier that separates the circulating blood from the brain extracellular fluid in the central nervous system. The bloodbrain barrier is formed by brain endothelial cells, which are connected by tight junctions with an extremely high electrical resistivity of at least 0.1 Ω m.96 Under normal conditions, the blood-brain barrier allows the passage of water, some gases, and lipid-soluble molecules by passive diffusion, as well as the selective transport of molecules such as glucose and amino acids that are crucial to neural function. Many pathologic conditions, including stroke, ischemia, tumors, AVMs, seizures, as well as metabolic and infectious encephalopathies, can damage this friable barrier, increasing the permeability to fluids and solutes, and they may contribute to brain swelling and raised ICP. Hence caution needs to be exercised with regard to the choice of intravenous fluids and their osmolarity in neurosurgical patients.

Solutions for Intravenous Use The term crystalloid refers to solutions that have an oncotic pressure of zero. Crystalloids may be hyperosmolar (mannitol, hypertonic saline), hypo-osmolar (5% dextrose, lactated Ringer solution), or iso-osmolar (normal saline). The administration of a hypo-osmolar crystalloid such as 5% dextrose can result in excess free water leading to an increased ICP and an edematous brain. Conversely, the administration of markedly hyperosmolar solution such as mannitol leads to a decrease in brain water content and ICP. The term colloid denotes solutions with an oncotic pressure similar to that of plasma (approximately 280 mOsm). Some commonly administered colloids are 5% and 25% albumin, 6% hetastarch (Hespan), the dextrans, and plasma. Crystalloids are the most common intravenous fluids used in the perioperative period. Although colloids have been part of intraoperative fluid management, substantially higher costs prohibit their routine use.97 More important, the largest meta-analysis to date specifically examined the use of albumin (as opposed to grouping all colloids) and again reported that

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there was no difference in outcome for patients treated with albumin compared with crystalloids.98 For the majority of simple elective craniotomies, crystalloids are adequate. However, in situations requiring substantial volume administration, a combination of isotonic crystalloid and colloid may be appropriate. Colloids are particularly beneficial in long spinal instrumentation surgeries where they are used to substitute blood loss and help prevent postoperative generalized body swelling (related to prone positioning) and swelling of the airway. The various starch-containing solutions should be used cautiously in neurosurgery because, in addition to a dilutional reduction of coagulation factors, they interfere directly with both platelets and the factor VIII complex. Dextran may also interfere with blood typing and cross matching and in addition has the potential to cause renal failure. These adverse effects have limited the use of hetastarch and dextrans in neurosurgery. Human albumin is available for infusion in 5% and 25% solutions. Albumin has a molecular weight of approximately 69,000, constitutes 50% of the total plasma proteins by weight, and is responsible for 80% of the colloid osmotic pressure of plasma. For these reasons and due to its lack of side effects on coagulation, albumin is considered a useful volume expander in neurosurgical cases. However, the Saline versus Albumin Fluid Evaluation (SAFE) study, comparing albumin to normal saline fluid resuscitation in patients with traumatic brain injury, found that albumin was associated with higher mortality than saline.99 Goal-directed fluid therapy (GDT) may help in establishing fluid balance for an individual patient in the perioperative setting, with evidence of reduced postoperative morbidity supporting its use in many surgical settings. Traditional measurements do not have the ability to adequately identify and guide fluid therapy.100 Neither the central venous pressure number nor its rate of change accurately assesses blood volume or predicts the response to a fluid challenge.101 Less invasive methods of monitoring flow-based hemodynamic parameters have been developed. These include esophageal Doppler monitoring and arterial waveform analysis (stroke volume variation, pulse pressure variation). Other methods require both arterial and central venous access to measure cardiac output. Both the LiDCO and PiCCO systems use pulse contour analysis to measure stroke volume after initial calibration with either lithium (LiDCO) or thermal indicators (PiCCO).

Emergence From Anesthesia The emerging goals in neuroanesthesia are to (1) produce rapid awakening to facilitate neurologic evaluation; (2) generate smooth awakening to prevent coughing, bucking, and hypertension; (3) provide adequate postoperative analgesia; and (4) prevent postoperative nausea and vomiting. Management consists of short-acting anesthetic agents to achieve rapid awakening. It is important to make sure that muscle relaxants are adequately reversed to decrease the chance of postoperative hypoventilation or obstruction, which can increase the chances of cerebral edema due to hypercarbia. Many anesthesiologists commonly use intravenous lidocaine, remifentanil, or

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short-acting antihypertensives such as esmolol and nicardipine to provide a smooth awakening.102,103 In summary, successful management of anesthesia and neuromonitoring is critical to accomplish desirable outcomes after cranial and major spine surgery. Effective anesthetic management starts with preoperative evaluation and encompasses careful intraoperative management and planning for smooth recovery in collaboration with the multidisciplinary team of experts.

Selected Key References Chui J, Manninen P, Valiante T, et al. The anesthetic considerations of intraoperative electrocorticography during epilepsy surgery. Anesth Analg. 2013;117(2):479-486. D’Angelo V, et al. Propofol EEG burst suppression in carotid endarterectomy. J Neurosurg Sci. 2001;45(3):157-162. Devin CJ, McGirt MJ. Best evidence in multimodal pain management in spine surgery and means of assessing postoperative pain and functional outcomes. J Clin Neurosci. 2015;22:930-938. Lingzhong Meng MD, et al. Cardiac output and cerebral blood flow. The integrated regulation of Brain Perfusion in Adult Humans. Anesthesiology. 2015;123:1198-1208. Postoperative Visual Loss Study Group. Risk factors associated with ischemic optic neuropathy after spinal fusion surgery. Anesthesiology. 2012;116:15-24. Practice Advisory for Preanesthesia Evaluation. An Updated Report by the American Society of Anesthesiologists Task Force on Preanesthesia Evaluation. Anesthesiology. 2012;116(3):522-538. Practice guidelines for management of the difficult airway: an updated report by the American Society of Anesthesiologists Task Force on

Management of the Difficult Airway. Anesthesiology. 2003;98: 1269-1277. Practice guidelines for preoperative fasting and the use of pharmacologic agents to reduce the risk of pulmonary aspiration: application to healthy patients undergoing elective procedures. An updated report by the American Society of Anesthesiologists Committee on Standards and Practice Parameters. Anesthesiology. 2011;114:495-511. SAFE Study Investigators. Saline or albumin for fluid resuscitation in patients with traumatic brain injury. N Engl J Med. 2007;357(9): 874-884. Sharma D, Lam AM. Neuroanesthesia: Preoperative Evaluation. Youmans’ Neurological Surgery. 6th ed. Philadelphia: Elsevier; 2011. Sharma D, Siriussawakul A, Dooney N, et al. Clinical experience with intraoperative jugular venous oximetry during pediatric intracranial neurosurgery. Paediatr Anaesth. 2013;23(1):84-90. Strebel S, Lam AM, Matta B, et al. Dynamic and static cerebral autoregulation during isoflurane, desflurane, and propofol anesthesia. Anesthesiology. 1995;83(1):66-76. Todd MM, et al. Mild intraoperative hypothermia during surgery for intracranial aneurysm. Intraoperative Hypothermia for Aneurysm Surgery Trial (IHAST) Investigators. N Engl J Med. 2005;352(2): 135-145. Yagi M, Hasegawa J, Nagoshi N, et  al. Does the intraoperative tranexamic acid decrease operative blood loss during posterior spinal fusion for treatment of adolescent idiopathic scoliosis? Spine. 2012;37: E1336-E1342. Zhang F, Wang K, Li F-N, et al. Effectiveness of tranexamic acid in reducing blood loss in spinal surgery: a meta-analysis. BMC Musculoskelet Disord. 2014;15:448-456. Please go to ExpertConsult.com to view the complete list of references.

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102.e2

PART 1

General Overview

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