A BIWEEKLY PUBLICATION FOR CLINICAL NEUROSURGICAL CONTINUING MEDICAL EDUCATION

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Cortical Mapping in the Resection of Gliomas

Part II: Anesthetic Considerations

Vikram C. Prabhu, MD, Cesar Vargas, MD, William J. Benedict, Jr., MD, Kevin Owen, MD, and W. Scott J ellish, MD, PhD

Learning Objectives: After reading this article, the participant should be able to:

1. Describe the use of anesthetic medications in cortical mapping procedures.

2. Explain airway management issues in awake craniotomies.

3. List the principles governing administration of a scalp block for an awake craniotomy.

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This article is the second of three parts.

Cortical mapping under monitored anesthesia is an effective way to reduce the morbidity associated with surgery for lesions in proximity to eloquent parts of the brain. The goal is to achieve a controlled and reversible depression of the central nervous system, with analgesia, while maintaining adequate spontaneous ventilation. The patient must be safe and comfortable, experiencing minimal anxiety, and able to wake up quickly to an alert cooperative state so that neurological testing can be done.

Conscious sedation initially was introduced for the resection of epileptic foci near the language or motor cortex, and the technique used both topical scalp anesthesia via local anesthetics (LAs) and IV medications. The technique of neuroleptic anesthesia involved the use of a potent sedative and an opioid to achieve a relaxed, pain-free state. Droperidol and fentanyl were the main agents used for this purpose, but uncontrolled and excess sedation and a high incidence of intraoperative seizures were serious limitations. The advent of short-acting sedatives such as propofol provided a means of administering sedation in a

Dr. Prabhu is Assistant Professor, and Dr. Benedict is Chief Resident, Depa.rtment of Neurological Surgery; and Dr. Vargas is Instructor, Dr. Owen is Resident, and Dr. [ellish is Professor and Chairman, Department of Anesthesiology; Loyola University Medical Center, 2160 South First Avenue, Maywood, TL 60153; E-mail: vprabhu@lumc.edu.

The authors have disclosed that they have no significant relationships with or financial interests in any commercial organizations pertaining to this educational activity.

Lippincott CME Institute, Inc., has identified and resolved all faculty conflicts of interest regarding this educational activity.

controlled fashion. Combined with opioids such as fentanyl or remifentanil, these drugs were found to meet the needs for cortical mapping surgery and to be well tolerated by patients, leading to more widespread use.

Historically cortical mapping procedures have been well tolerated with no notable physiological or psychological sequelae. They usually are performed for tumor or epilepsy foci resections in patients ranging in age from 11 to 71 years. Scalp and dural anesthesia along with IV sedatives, analgesics, and inhalational agents is used. However, patients undergoing cortical mapping procedures are exposed to unique risks, and anticipating and preventing these problems is essential. Pain, emotional distress, or hypertensive spikes may occur during head pin placement and frame immobilization. A patient may feel uncomfortable being immobilized for a prolonged time or claustrophobic under thick surgical drapes. Patients may experience headache, nausea, vomiting, or seizures. The major concern, however, is the profound respiratory depression that may accompany the use of analgesics and sedatives in the doses required to obtain cranial access without discomfort or pain. Hypoventilation may lead to hypoxia or hypercarbia, which may aggravate pre-existing cerebral edema. Urgent airway access may be difficult to obtain with the head immobilized, should airway obstruction or respiratory depression persist. It is crucial for surgeons performing these operations to understand the anesthetic issues. In this second part of

Category: Tumor

Key Words: Awake craniotomy, Scalp anesthetic block, Conscious sedation

a three-part article, we delineate our anesthetic protocol and describe the appropriate use of ]V and inhalational anesthetics, as well as important airway management principles that arc essential for the safe conduct and successful completion of a cortical mapping procedure.

Sedatives and Analgesics

Smooth anesthetic technique begins in the preoperative stage. Surgical procedures such as cortical mapping may provoke tension or fear in the patient; anxiety can produce myriad symptoms including palpitations, tachycardia, chest pain, sweating, pallor, headache, nausea, or difficulty concentrating, all of which may compromise the operation. Hence, carefully preparing the patient for surgery and providing reassurance is essential and, in most cases, adequate. In some patients, however, premedication with anxiolytic agents such as benzodiazepines may be considered. Benzodiazepines, which act on the gamma-aminobutyric acid (CABA),\-chloride channel receptor complex, are mildly sedating in addition to their anxiolytic functions. Diazepam (Valium; Roche Laboratories), 5 to 10 mg PO, or midazolam (Versed; Roche Laboratories), 2 to 4 mg IV, is commonly used. Clonidine (Catapres; Boehringer Ingelheim) is an antihypertensive medication that sometimes is used before surgery. Given in a dose of 0.1 to 0.2 mg PO, it can induce mild sedation and confer hemodynamic stability by blunting the adrenergic response. It also has mild analgesic properties.

At surgery, our protocol combines a sedative such as propofol with a narcotic analgesic such as remifentanil, both of which are short-acting agents. Propofol (Diprivan; AstraZcneca) is a sedative-hypnotic that activates GABA receptors and has a short half-life, making it easy to titrate and permitting prompt awakening after the IV infusion is stopped. It has antiemetic and anticonvulsant properties and is cleared rapidly by hepatic and extrahepatic metabolism. It also has amnestic properties; most patients have no recollection of the operation. Side effects arc rare but include occasional pain on injection or bradycardia. Infection is not a major concern and is a risk only with long-term (>24 hours) infusion of this agent. Combined with fentanyl or remifentanil, propofol provides

EDITOR: Ali F. Krisht, M.D!

University of Arkansas for Medical Sciences

ASSISTANT EDITOR: Cargill Alleyne, Jr., M.D.' Medical College of Georgia

PRODUCTION ASSISTANT: Ronalda Williams EDITORIAL BOARD:

Sadih Adada, M.D. Ossama AI-Melty, M.D. Rick Soop, M.D.

Evandro de Oliveira, M.D. Allan Friedman, MD. Gerardo Guinto, M.D. Douglas Kondziolka, M.D. Jacques Marcos, MD. Tom Origitano, MD. Nelson Oyesiku, MD. Kalman Post, MD. Richard Rowe, M.D. Martin Weiss, MD.

M. Gazi Ya~argil, MD.

, Dr. Krisht has disclosed that he has no significant relationships with or financial interests in any commercial organizations pertain ing to this educational activity. Dr. Alleyne has disclosed that he is a consultant for Cordis.

excellent sedation, analgesia, and seizure control without any compromise of cognitive function. The infusion is titrated so that the initial, painful part of the operation is performed without the patient experiencing any discomfort or awareness. The main concern with propofol is respiratory depression, especially when it is combined with opioids, so pulse oximetry and capnography are essential accompaniments, along with a patent airway. If ventilatory or hemodynamic problems OCCUl~ the propofol infusion is stopped; typically, the effects wear off rapidly. Naloxone (Narcan: Endo Pharmaceuticals, Inc.), 20 to 40 pg IV, is administered to reverse the effects of the opioids. Propofol initially was introduced for use in epilepsy surgery, but its anticonvulsant property may suppress electroencephalographic (EEe) recordings, typically in a burst suppression pattern.

More recently, dexrnedetomidine (Precedex: Orion Corp.), a central-acting, highly selective alpha=adrenergic agonist, has emerged as an alternative to propofol. Dexmedetomidine ini tially "vas approved by the FDA in 1999 for shortterm «24 hours) sedation in intensive care units. Infusions of this drug provide sedation similar to natural sleep due to a unique action on the pontine locus ccruleus, which is an important modulator of Vigilance. After the infusion is stopped, patients are easily aroused simply by talking to them. Only minimal respiratory depression is noted. Analgesic properties stem from the drug'S action on alphajadrenergic receptors in the dorsal horn of the spinal cord. An amnestic effect also is noted. Side effects of dexmedetomidine are attributed primarily to its sympatholytic and vagomimetic properties and include hypotension and bradycardia. In most cases, these side effects can be avoided by careful titration of the drug, but they can pose a problem in patients with an occult cardiac conduction block or high vagal tone. Transient hypertension due to peripheral vasoconstriction following bolus injection of dexmedetomid ine also may occur.

Opioid analgesics such as fentanyl (Sublimaze: Akorn, Inc.) and rernifentanil (Ultiva: Abbott Laboratories) are useful adjuncts to these sedatives. Fentanyl is 75 to 100 times more potent than morphine and is highly lipid-soluble, with

The continuing education activity in Contempomry Neurosurgery is intended for neurosurgeons, neurologists. neuroradiologists. and neuropathologists.

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~ ~--~---~------------

a rapid onset of action in 5 to 10 minutes. It does not cause histamine release and may suppress the stress response. Although significant hemodynamic effects are uncommon, bradycardia and hypotension occasionally may occur due to its effect on carotid baroreceptors. Continuous infusion may improve the analgesic effect of fentanyl, but it also depresses ventilation more significantly. The potency of remifentanil is similar to that of fentanyl, but it acts more quickly and has a very short half-life, because it is metabolized rapidly by nonspecific plasma cholinesterases, When a remifentanil infusion is stopped, patients wake up rapidly, typically in 5 to ] 0 minutes. Side effects are consistent with other opioids and include nausea, vomiting, and decreases in blood pressure and heart rate. The major concern is the increased risk of respiratory depression when used with propofol,

Inhalational Agents

Inhaled anesthetics often are used to supplement the medications discussed in the preceding section. These drugs depress neuronal activity by altering sodium influx and raise the threshold for individual neurons to fire. The central nervous system depression is reversible and does not cause prolonged impairment of intellectual and cognitive function. The efficacy of these agents is measured by their blood:gas partition coefficient and minimum alveolar concentration (MAC). The blood-gas partition coefficient is an index of the solubility of the agent and reflects its induction and emergence times. The MAC is defined as the alveolar partial pressure of a gas at which 50% of humans will not respond to a surgical incision and is a measure of the potency of the agent.

The most commonly used inhalational agent for cortical mapping cases is sevoflurane (Ultane; Abbott Laboratories), a fluorinated methyl-isopropyl ether anesthetic with a low blood:gas partition coefficient that allows for rapid induction and quick recovery after discontinuation of the agent. It is nonpungent, and airway irritation is minimal (the least among clinically used volatile anesthetics). It is our preferred inhalational agent and is combined with opioids such as fentanyl or rernifentanil to provide a level of sedation that permits administration of the scalp block and immobilization in the Mayfield headholdcr,

Other inhalational anesthetics include desflurane (Suprane:

Baxter Healthcare Corp.). isoflurane (Forane: Ohio Medical Products), and halothane (Fluothane: Wyeth-Ayerst). Desflurane is a fluorinated methyl-ethyl ether with a lower blood:gas partition coefficient than sevoflurane, which translates into even more rapid induction and awakening after discontinuation. It often is used for short proced ures in outpa tient surgery centers. The problem with desflurane is its pungency which produces airway irritation that can cause patients to experience appreciable salivation, breath holding, coughing, or even laryngospasm, making it unsuitable for use during cortical mapping.Isoflurane is a halogenated volatile anesthetic agent that often is used for general anesthesia. Like desflurane, it is pungent and can cause coughing and salivation. Most importantly it is a profound respiratory depressant, particularly when administered with a narcotic medication. Consequently it has no potential for use in cortical mapping. Halothane is n011- pungent and is well tolerated, but it has poor analgesic prop-

erties and causes depression of cardiovascular and respiratory function. It no longer is used routinely for general anesthesia and is unsuitable for awake mapping procedures.

In most cases, after the inhaled anesthetic concentration reaches 0.4 MAC, patients will not respond to commands or painful stimuli. This level of anesthesia suffices for the initial part of the procedure, but inhalational concentration usually must be increased or propofol or dexmedetomidine must be added to maintain a level of sedation that will permit the cranial and dural opening. Increasing the inhaled anesthetic dose to more than 0.6 MAC may deepen sedation, but it could produce cerebral vasodilation and decreased cerebral vascular resistance with increased cerebral blood flow, which may increase intracranial pressure (rCF). In intubated patients, this increase in ICP is attenuated by hyperventilating the patient, but this may not be feasible in a spontaneously breathing, nonintubated patient.

Antiepileptic Agents

Intraoperative seizures occur either spontaneously or as a result of stimulation, and they may be either clinically obvious or detected only on EEG recording. Most are selflimiting and cease after the stimulation is stopped. Persistent seizures can be stopped by dripping ice-cold Ringer's lactate onto the exposed brain. For refractory seizures, midazolam 2 mg IV is administered; a metabolic panel, arterial blood gas, and serum anticonvulsant levels are checked. If anticonvulsant levels are subthcrapeutic, additional drug is administered. Fosphenytoin (Cerebyx: Pfizer, Inc.) 20 mg/kg phenytoin equivalents, 150 mg/minute IV, is COI1lmonly used. Patients allergic to phenytoin/fosphenytoin may be treated with phenobarbital, diazepam, or lorazeparn (Ativan: Baxter Healthcare Corp). Seizure activity that persists for more than 15 minutes constitutes status epilepticus and is a medical emergency. Should this occur, in addition to the measures already described, the patient should be removed from the headholder and the airway should be controlled with either a laryngeal mask airway (LMA) or an endotracheal tube.

Midazolam is an excellent drug for rapid control of intraoperative seizures refractory to the application of ice-cold Ringer's saline. Itis kept readily available throughout the procedure. Midazolam is two to three times more potent than diazepam because of its greater affinity for the benzodiazepine receptor, and it also has an amnestic effect. The onset of action after a 1- to 2-mg IV dose occurs within 30 to 60 seconds, with sedation lasting 15 to 80 minutes (or longer, in elderly patients). The main concern, again, is depression of ventilation and resultant hypoxia, which is exaggerated by concomitant use of opioids or sedatives. Hence, airway C011- trol is important when this drug is administered.

Local Anesthetics

Local anesthetics block nerve conduction by inactivating transmembrane sodium channels, providing a reversible painfree zone in infiltrated areas. These drugs consist of a lipophilic benzene ring and a hydrophilic amino group separated by a hydrocarbon chain. The link between the hydrocarbon chain and the benzene ring is an ester or amide bond that distinguishes

3

Table 1. Guidelines for Local Infiltrative Anesthetic Dosing'

Local Anesthetic

Dose (mg/kg) With Epinephrine 1 :200,000

Dose (mg/kg) Without Epinephrine

Lidocaine 1 % Bupivacaine 0.5%

5 mg/kg 3 mg/kg

7 mg/kg 3 mg/kg

'Dosing per kg up to a maximum of 100 kg. Palienls weighing more than 100 kg should be dosed at the rate for 100 kg.

two classes of anesthetics with distinct properties. Cross-sensitivity between the two groups usually does not OcCUl~ but it may occur among drugs in the same class. Allergic reactions are more common with ester LAs. They are metabolized to p-aminobenzoic derivatives, which may cause hypersensitivity reactions such as urticaria or bronchospasm. Allergic reactions to amide LAs, which we usually use, are rare but they occur occasionally due to the added preservative methylparaben. Ester anesthetics are metabolized by plasma cholinesterases, most commonly pseudocholinesterase. Amide anesthetics, on the other hand, are metabolized by microsomal hepatic enzymes, and the dose is reduced in Figure 1. Illustration showing cutaneous nerve supply of the scalp and sites of local anesthetic

patients with liver dysfunction. administration.

Absorption of an LA depends on

concentration, addition of epinephrine, and local tissue vascularity. When epinephrine, a vasoconstrictor, is added to an LA, it limits systemic toxicity, decreases tissue bleeding, and prolongs its duration of action. LA solutions containing epinephrine are not used in areas supplied by end arteries such as digits, ears, nose, or penis because there is a risk of ischemia, but this is not an issue with scalp blocks. Care also must be taken to prevent accidentallV injection of LAs supplemented with epinephrine, especially in a patient with known or suspected cardiac arrhythmia.

Local tissue toxicity with LAs is rare and usually is reversible. Cardiac toxicity from LAs results from sodium channel inactivation and manifests as conduction abnormalities that may progress to arrhythmias and hypoxia. Hypercarbia, acidosis, or hyperkalemia aggravates these effects. Central nervous system toxicity may result from inadvertent IV or intra-arterial administration and manifests as light-headedness, dizziness, blurry vision, metallic taste, tinnitus, tremors, nystagmus, shivering, tonicoclonic seizures, or respiratory depression. The key is to maintain a patent airway, optimize oxygenation, minimize hypercarbia, and maintain hemodynamic stability with IV fluids and pressor agents. Seizures can be managed with benzodiazepines such as IV diazepam or midazolarn.

These general concerns aside, epinephrine-supplemented LAs serve well in scalp topicalization for awake craniotomies. Lidocaine (Xylocaine: AstraZeneca) and bupivacaine (Marcaine: Hospira, Inc., or Sensorcaine: Astra.Zeneca) are amide anesthetics with relatively good potency that we use in combination for these procedures. Lidocaine has a

Au riculotemporal nerve

rapid onset and moderate duration of action, lasting 1 to 2 hours. Bupivacaine acts more slowly but its effects last longer, typically 2 to 6 hours, depending on the concentration and the addition of epinephrine. However, bupivacaine has the potential for cardiotoxicity, especially when used in a concentrated solution or in large volumes. Ropivacaine is an alternative agent with low toxicity and long duration of action that has been used successfully in obstetric cases, but we have no experience with its use.

When a patient reports pain during the procedure, it usually is due to ineffective scalp or dura topicalization or paucity of sedative and opioid use. It is essential to dose and administer the LAs appropriately to maximize patient comfort and decrease requirements for IV medications. A mix of 1°/..) or 2'X, lidocaine with 1 :200,000 epinephrine (4.5 ml.), 0.5% bupivacaine with 1:200,000 epinephrine (4.5 ml.), and 8.4% sodium bicarbonate (1 ml.) is loaded in each 10-mL control syringe. The addition of sodium bicarbonate to the LA increases the proportion of the drug that is in the nonionized form and improves speed of onset because of better nerve membrane permeability. The total dose of an LA is calculated based on a mg/kg dosage scheme (Table 1), and cutaneous nerves are targeted to obtain an analgesic zone that encompasses the scalp and cranial opening (Pigure l ).

The trigeminal nerve (cranial nerve V) and cervical plexus supply cutaneous sensory innervation to the face, head, and neck. The ophthalmic division of cranial nerve V supplies the forehead, eyebrows, and upper eyelids via the supraorbital and supratrochlear nerves. The supraorbital nerve emerges from the supraorbital notch at the junction of the

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IV line

Avoid lines

[········~·······~~·····~~··~·~l

Suction.

cautery equipment

............ _ ..... --.-- ... _ ...

c · · .. · ·j

Neurophysiologist with monitoring equipment

_ .. _-_._ ... _._ .... __ .. _._ ...

Figure 2. Illustration showing operating room set-up for cortical mapping procedure (Loyola University Medical Center, Maywood, IL). N, nurse; 8, surgeon; SA, surgical assistant.

lateral two thirds and medial one third of the superior orbital rim in a vertical line with the pupil and the eye in neutral position. The supratrochlear nerve emerges just medial to it. The greater occipital nerve from the posterior rami of C2-C4lies about midway between the mastoid process and the inion, next to the occipital artery. The lesser occipital nerve and great auricular nerve are lateral to it. Together, these nerves supply the scalp over the posterior occipital, parietal, and temporal regions. The zygomaticotemporal and auriculotemporal nerves, branches of the maxillary and mandibular divisions, respectively, of cranial nerve V supply the lateral scalp over the frontal and temporal areas.

Airway Management

Before surgery, the anesthesiologist must determine whether the patient's airway is compatible with the pro .. posed procedure and assess whether the patient will be able to breathe spontaneously and adequately while sedated. Medical history and anesthesia records provide information regarding disease states with complicated and difficult airway management or poor tolerance to respiratory depression. The degree of mouth opening, loose or protruding teeth, or a large tongue are important considerations. The presence of a beard or an unusually large nose may make

mask ventilation difficult. Neck mobility is assessed, and the presence of neck masses or tracheal deviation is checked. A thy rom ental distance of 5 to 6 em is desirable, as is good extension at the atlanto-occipital joint. Morbid obesity, chronic obstructive pulmonary disease (COPD), and cardiac disease are important comorbid conditions that may preclude an awake cranial operation.

At surgery, the patient is positioned either supine or with the back elevated 30 to 40 degrees, which facilitates respiratory excursions (Figure 2). A face mask of appropriate size is used and secured with straps, ensuring a tight seal. When the head is secured in the Mayfield head holder, the chin and mandible are lifted up in a partial "sniff" position, maintaining airway patency by aligning the oral, pharyngeal, and laryngeal axes. This position prevents airway obstruction by the tongue. Upper airway patency is maintained with a nasal airway (32-Fr or the highest caliber permissible) coated with lidocaine jelly. The lower airway begins at the vocal cords, and any obstruction or disease at or below that level is not compatible with an awake procedure. Problems such as obstructive airway disease (e.g., severe asthma or severe COPD), tracheal stenosis, mediastinal mass, goiter, or any obstructive element below the vocal cords require intubation; extubation for neurological testing is not an option, because it is associated with a high risk of respiratory compromise.

r Difficult Airway ~

Anticipated or recognized Unanticipated or recognized

preoperatively during surgery

• +

Sleep-awake-sleep airway controlled using LMA

Stop

a nesthetics/sedati vesl reverse narcotics

+

Jaw thrust

+

Place oral or nasal airway

+

Place LMA

t

Remove from head holder

t

Place oro- or nasotracheal tube with laryngoscope

t

Place oro- or endotracheal tuve

with fiber optic scope

t

Tracheostomy or cricothyroidotomy

Figure 3. Algorithm for sequential emergency airway management LMA, laryngeal mask airway.

5

Table 2. Ramsay Scale

Level Patient Characteristics

Awake, anxious, aqitated, or restless

2 Awake, cooperative, oriented, and tranquil

3 Drowsy, with response to commands

4 Asleep, brisk response to glabella tap or loud auditory stimulus

5 Asleep, sluggish response to stimulus

6 No response to firm nail-bed pressure or other noxious stimuli

Spontaneous ventilation is verified by monitoring the endtidal carbon dioxide waveform (ETC02). Capnography continuously monitors the patient's inhaled and exhaled concentrations of carbon dioxide. The displayed waveform provides information about the rate of respiration and patient's ability to exchange air. It is a sensitive marker for hypoventilation and apnea, which could occur from oversedation, The apnea could be due to obtundation of respiratory drive or obstruction of the airway. The capnograph also provides information regarding the success of efforts to improve ventilation or rescue the airway in case oversedation and apnea secondary to obstruction occur. Pulse oximetry alone cannot ensure that the patient is ventilating, because it may remain in the normal range for several minutes after apnea occurs secondary to apneic oxygenation.

In the event of airway obstruction or ventilatory compromise, a simple algorithm is followed (Figure 3). A decrease in ETC02, or oxygen saturation, or an audible airway obstruction should initiate a jaw thrust maneuver to re-establish a patent airway. IV sedation and analgesic infusions are stopped and pharmacologically reversed if needed. Although the patient's head is immobilized, the mandible continues to have free range of motion. The jaw thrust is done by placing the base of the thumbs over the zygomatic arches and the fingers behind the angle of the jaw. Bringing the jaw forward displaces the tongue from the posterior pharyngeal wall. If this maneuver is not adequate, an oral airway is inserted, especially if the tongue is the main obstructing element. An oral airway establishes patency by lifting the tongue and epiglottis aW(ly from the posterior pharyngeal wall. If spontaneous ventilation is still lacking or if airway obstruction persists, an LMA is placed.

At this point in the procedure, airway management options do not preclude resumption of the neurosurgical operation after respiratory function is stabilized and adequate and spontaneous ventilation resumes. We have not yet encountered a case in which we needed to test any steps of the algorithm after the jaw thrust maneuver. If, however, these maneuvers are unsuccessful and respiratory compromise continues, the surgical procedure probably should be terminated by closing the scalp rapidly over a dural substitute without replacing the bone flap and releasing the patient's head from the headholder pins. An endotracheal tube should be inserted and mechanical ventilation performed. If endotracheal or nasotracheal intubation fails, an emergency cricothyroidotomy or tracheostomy would be the next option.

Patients in whom airway concerns are anticipated or recognized prior to surgery may be candidates for a "sleep-

.-------~-------- .. - .. ~ .. -.~.-'- .. -.~.'-.----

awake-sleep" technique that uses an LMA to protect the airway. General anesthesia is induced with IV medications (usually propofol, fentanyl, or remifentanil) with or without inhaled anesthetics, and an LMA is introduced. Approximately 20 minutes prior to testing, the inhaled anesthetics are turned off, IV anesthetics are reduced, and the LMA is removed. After testing is complete, general anesthesia is re-induced and the LMA is replaced for the remainder of the procedure. This technique optimizes patient safety and comfort during the most stimulating portions of the surgery (i.e., incision and reflection of the scalp, bone flap removal, and dural manipulation) and avoids potentially devastating respiratory depression. Placement of an LMA obviates the need for laryngoscopy and head extension and is accomplished easily even if the patient is in a difficult position. Although coughing and gagging during emergence from anesthesia and removal of the LMA may occur, usually due to accumulation of saliva, it can be attenuated by administration of glycopyrrolate, 0.2 to 0.4 mg IV, before placement of the LMA and suctioning the airway prior to its removal.It also may be helpful to remove the LMA with the cuff inflated or partially inflated, because it may clear excess saliva upon its removal.

The Anesthesia Sequence

Admission the night before the procedure ensures a rested patient and provides the opportunity to ensure that all necessary imaging and laboratory studies have been obtained, review airway issues, and counsel the patient regarding the operation. IV dexamethasone (Decadron: Merck & Co., Inc.) 6 mg IV q6h is administered. Therapeutic antlepileptic medication levels are ensured. Premedication is not routine but occasionally is used.

The patient is positioned in a comfortable reclining position with adequate padding in an operating room with normal ambient temperature (Figure 2). A good rapport between team members instills confidence in the patient. A standardized setup that accommodates equipment and personnel and maximizes sterility and safety is important. TV access is secured and monitors are placed. The face mask is secured with straps, ensuring a tight seal. Adequate length of IV lines and other tubing is essential, as the head end of the bed is rotated 180 degrees away from the anesthesiologist. Continuous hemodynamic and respiratory function monitoring is routine. After adequate pulse oximetry and ETC02 readings are confirmed, sedation commences, and adequacy of ventilation is assessed. The face mask is replaced with a simple nasal cannula secured to the patient's face with tape, and continuous oxygen is administered at 2 to 6 L/minute. Sedation is deepened to Ramsay scale 4 or 5 (Table 2). Scalp topical anesthesia is administered. The head is secured in the Mayfield headholder, turned opposite to the side of the craniotomy, and the chin and mandible are lifted up in a partial "sniff" position. The headholder pins are sterile and coated in 1%, lidocaine jelly. A nasal airway (32-Fr or highest caliber permissible) covered with 1% lidocaine jelly is inserted. Neuronavigation registration is completed and accuracy is confirmed. The surgical site is prepped and draped per standard surgical principles with care to keep the drapes off the patient's face. Spontaneous ventilation is verified by monitoring of the ETC02leveis and

6

capnograpby. A propofol infusion (25-100 pg/kg/minute) is started, and rernifentanil (0.0625-0.25 pg/kg/minute) is administered. Patients refractory to sedation with these agents receive sevoflurane by mask. The depth of sedation is judged by the eyelash reflex, respiratory rate, and the patient's response to painful stimuli. After the patient is determined to be adequately sedated, a Foley catheter coated with 1%) lidocaine jelly is inserted and connected to a closed system drainage bag. An LMA, laryngoscope, and endotracheal tube are kept readily available. Infusions of propofol and remifentanil are titrated to a Ramsay sedation level of 6 with the goal of maintaining the respiratory rate above lO/minute and oxygen saturation above 95'};). No paralytic agents are used at any point during the procedure. Mannitol 0.25 g/kg IV dexamethasone 10 mg IV and prophylactic antibiotics are administered prior to surgical incision.

Following scalp and cranial bone opening, the middle meningeal artery is identified and coagulated, and 1'X, lidocaine with] :200,000 epinephrine is administered between the leaves of the dura adjacent to it. At the surgeon's cue, the propofol infusion is turned off, generally 20 to 30 minutes prior to cortical mapping. The goal is Ramsay level 2 with the patient cooperative, tranquil, and oriented. Wake-up time varies from 5 to 15 minutes and occasionally may take up to 30 minutes. Ondansetron (Zofran; GlaxoSmithKline) 4 mg IV and occasionally remifentanil is administered, because surgical contact with cranial base dura may cause pain, nausea, or vomiting. Midazolam 2 mg for IV administration is kept available in the event of seizures. Gelfoam pledgets (Pharrnacia & Upjohn) soaked in lidocaine 1% with 1 :200,000 epinephrine are laid on the dura and are effective in minimizing pain from contact with this structure. After the mapping and tumor resection are C0111-

plete, the patient is re-scdated with propofoJ at a lower dose US-30 pg/kg/minute) for the remainder of the procedure. On average, the patient is awake for approximately 45 to 60 minutes, and the entire surgical procedure lasts 4 to 6 hours.

Acknowledgements. The authors thank Dianne Mattia for creating the illustrations; Steven Edelstein, MD, for reviewing the text; and Julius Pawloski, MD, for providing the dosing schedule in Table 1.

Ard j, Doyle W, Bekker A. Awake craniotomy with dexmcdetomidine in pediatric paticnts.J Nell mSIl rg Al1fSIIICsioI15:263, 2003

Bekker A, Sturaitis MK. Dcxrnedctomidine for neurological surgery. NeIlI"OsUlgery 57(ONS suppll): 1, 2005

Borkonstadt H, Ram Z. Monitored anesthesia care in awake craniotomy for brain tumor surgery. lsr Med Assoc J 3:297, 2001

Blanshard HI, Chung l~ Manninen PH, ct al, Awake craniotomy for removal of intracranial tumor: considerations for early discharge. Anesth Alwlg 92:89,2001

Danks l{A, Rogers M, Aglio L, et al. Patient tolerance of craniotomy performed with the patient under 10m I anesthesia and monitored conscious sedation. NeII/"OsUlgery42:28, 1998

Keifer JC DenIchcv D, Little K, et al. A retrospective aualysis of a remifentanil I propofol general anesthetic for craniotomy before awake functional brain milpping. Alles/Ii Anllig 1(l"l :502, 2005

Mi1Ck PI;; Perrine K, Kobylarz E, ct al, Dexmcdctomidine and ncurocognilive testing in awake craniotomy. J NeurosUlg AllcslilesioI16:20, 2004 Manninen PH, Balki M, l.ukitto K, Bernstein M. Patient satisfaction with awake craniotomy for tumor surgery: a comparison of romifontanil and fentanyl in conjunction with propofol, Anestl: Aiwig 102:237, 2006 Sar<mg A, Dinsmore j. Anaesthesia for awake craniotomy: evolution of a techniquc Ihilt facilitates awake neurological testing. I3r} Anneslli 90:16], 20D3 Skucas AI', Artru AA. Anesthetic complications of awake craniotomies for epilepsy surgery. Allesl/l AUillg 102:882, 2006

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1. Risks associated with awake craniotomy procedures include pain, emotional distress, and hypertensive spikes during head pin placement and frame immobilization; excess sedation causing hypoventilation and hypoxemia; and difficulty obtaining urgent airway access.

True or False?

2. Propotol is popular for conscious sedation procedures because it is easy to titrate, with prompt awakening after the IV intusion is stopped; and it has antiemetiC, amnestic, and anticonvulsant properties.

True or False?

3. Dexmedetomidine is a centrally acting, highly selective and specific atpha.-adrenerqic agonist used for short-term sedation in intensive care units that provides sedation similar to natura! sleep without depression of ventilation.

True or False?

4. Fentanyl does not cause nausea or vomiting and does not adversely affect the ventilation and hemodynamic status of the patient.

True or False?

5. Desflurane is associated with rapid induction and prompt awakening after discontinuation, but a disadvantage is its pungency, which produces airway irritation, salivation, breath holding, coughing, or laryngospasm.

True or False?

6. Midazolam depresses ventilation due to a decrease in the hypoxic drive, which is exaggerated by concomitant use of opioids or other central nervous system depressants.

True or False?

7. Lower airway obstruction or disease is not a contraindication to an awake craniotomy procedure.

True or False?

8. Absorption of a local anesthetic depends on local tissue vascularity and concentration of the drug, and the addition of epinephrine enhances local uptake, limits systemic toxicity, decreases tissue bleeding, and prolongs duration of action.

True or False?

9. Central nervous system toxicity may be seen as a result of inadvertent IV or intra-arterial administration of local anesthetics, and it manifests as light-headedness, dizziness, blurry vision, metallic taste, tinnitus, tremors, nystagmus, shivering, tonicoclonic seizures, or respiratory depression.

True or False?

10. Sedative infusions are stopped 20 to 30 minutes prior to cortical mapping, with the goal being a Ramsay level 2 state (i.e., cooperative, tranquil, oriented).

True or False?

8