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Awake Craniotomy, Epilepsy, Minimally Invasive and Robotic Surgery
Awake craniotomy
Awake craniotomy refers to surgery that is performed on the brain while the patient is in a state of awareness and that allows for cooperation with functional testing of the cortex. It is usually performed when eloquent cortical tissue—tissue that is involved in motor, visual, or language function—is located in close proximity to the area to be resected. This may include resection of tumor or ictal foci in patients with epilepsy. The patient’s awake state allows for the mapping of the brain near the area to be resected, which avoids morbidity related to resection of the eloquent tissue and can reduce anesthetic interference with brain mapping.
Awake craniotomy has been shown to reduce the size of the resection, surgery time, postoperative neurologic deficits, early postoperative nausea and vomiting, and hospital stay. Vasopressor use and hypertension during head pinning are also decreased. Hospital stays have been reported to be as short as 1 day for patients with good functional status and uncomplicated tumors. , Lower post-intensive care unit inpatient costs were found in patients undergoing glioma resection under sedation versus general endotracheal anesthesia. Awake craniotomy has even been studied as a potential outpatient procedure with no reported adverse outcomes. This technique has been shown to have better patient acceptance. Despite the most common complaints about pain from the head holder, inadequate local anesthesia, and uncomfortable position, patients report better postoperative pain scores and use less opioids in recovery.
The anesthetic technique for awake craniotomy varies. The common goal is to ensure the best possible resection by keeping patients comfortable and safe with sedation and anesthesia before and after the awake interval, and by monitoring and guiding patients through conscious mapping and testing. General anesthesia—using a laryngeal mask airway (LMA), endotracheal intubation, or varying degrees of sedation—with discontinuation of anesthesia for the period of speech, memory, or motor testing, or a combination of these techniques, has been described , and found to be safe.
Approach to the Awake Craniotomy
Appropriate patient selection and preparation are the most important factors in the success of anesthesia for awake craniotomy. In the selection process, the following should be considered: age and maturity; anxiety, claustrophobia, or other psychiatric disorders; a patent airway; and a history of reflux or nausea and vomiting. Literature and experience suggest that hypertension, alcohol abuse, and lack of maturity may be risk factors for sedation failure. We recommend that children younger than 14 years not be considered, although the developmental status of the individual should be assessed. Furthermore, a patient with a potentially difficult airway or who demonstrates that there is a likelihood that they will obstruct under sedation is a poor candidate for awake craniotomy. Because the patient’s head will be in pins and positioned by the surgeon, sudden conversion to endotracheal intubation may be difficult. A plan must exist between the anesthesia and surgical teams for the management of the airway should patency be lost. Patients with a history of obstructive sleep apnea (OSA), difficult ventilation, or difficult intubation may be considered as higher risk for adverse outcomes, although current evidence does not support OSA as an independent risk factor for failure of awake craniotomy.
Preoperative consultation is essential. The anesthesiologist should clearly outline for the patient what to expect during the procedure, including the varying states of sedation and awareness, the positioning, the possible discomfort, and the testing process. A strong rapport between the patient and the anesthesiologist should be established prior to the procedure, and comfortable patient positioning, scalp block, proper anesthetic selection, and communication are paramount. The anesthesiologist must keep in mind the psychological state of the patient and attempt to alleviate anxiety and discomfort as much as possible to ensure the success of the technique and the surgery.
Positioning
Patient comfort and access during the awake period is important in a successful awake craniotomy. Lateral or semi-lateral positioning is commonly used to allow for patient comfort and to offer the anesthesia team ideal access to the patient. Adequate padding and pillows should be provided and pressure points carefully checked. The patient should confirm an acceptable level of comfort prior to sedation, as he or she will be in pins upon emergence from sedation and must remain still during the period when repositioning is not feasible. The patient must also be positioned and draped for ideal access by the anesthesia team who need to speak with the patient to test motor and sensation. Tenting the drapes upward from the patient on the side of the anesthesia team provides an area of access and may also reduce the patient’s sense of claustrophobia. Fig. 17.1 shows a configuration for setup in the operating room. The patient’s position is stabilized with the use of a deflatable beanbag or a backrest fixed to the operating table, and the patient is taped to the table.
Scalp Block
Performance of a reliable blockade of the innervation of the scalp is essential to the successful performance of an awake craniotomy. The technique for local scalp block for craniotomy is well-described. , Individually blocking the auriculotemporal, zygomaticotemporal, supraorbital, supratrochlear, lesser occipital, and greater occipital nerves is necessary to provide complete analgesia of the scalp. Ropivacaine and levobupivacaine can be safely used up to doses of 4.5 mg/kg and 2.5 mg/kg, respectively. Mepivacaine may also be used adjunctively if a faster setup is required. These blocks achieve peak plasma concentrations approximately 15 minutes after injection. Severe bradycardia after scalp block has been reported.
If general anesthesia is performed for the initial asleep period, necessary access, invasive monitors, and urinary catheters may be placed after induction. However, if sedation is selected, it should be deep enough for the patient to comfortably tolerate these invasive measures with minimal recall. Scalp block may also be performed at this time. The success of the scalp block is likely not known until the placement of head pins begins. Obvious physical response in the sedated patient or an increase in heart rate and blood pressure in the general anesthesia patient would indicate block failure. Boluses of propofol may be necessary to temporarily rescue the inadequately sedated patient.
Anesthetic Options
A number of different anesthetic techniques may be useful for awake craniotomy. Some providers may choose varying levels of sedation as tolerated by the patient. Others may choose a general anesthetic, with or without endotracheal intubation, in what is referred to as the asleep-awake-asleep technique.
One may choose to perform a general anesthetic from induction to completion of exposure and awaken the patient for neurocognitive and neurofunctional testing. If this method is chosen, it is important to remember that the patient will be emerging in head pins and bucking must be avoided to prevent patient morbidity. Conversely, one may choose sedation during the exposure period, keeping in mind that airway reflexes should be preserved.
Propofol, dexmedetomidine, and opioid infusions have been safely and successfully used for awake craniotomy. Volatile anesthetics have been used for general anesthesia during the asleep portion of the procedure. While the patient is in head pins, the provider should be aware of the danger of laryngospasm during emergence and extubation or LMA removal.
Total intravenous anesthesia (TIVA) is a viable choice for awake craniotomy. Propofol-only anesthesia with spontaneously breathing patients has been described as safe. Propofol is begun with a bolus of 0.5 mg/kg and continued at a rate of 75–250 μg/kg/min. Practitioners have safely and successfully used a combination of propofol or dexmedetomidine with an opioid such as remifentanil, sufentanil, or boluses of fentanyl. The rapid clearance of remifentanil makes it an appealing choice for quickly achieving the awake state. However, remifentanil may cause hypopnea in the spontaneously ventilating patient. A dose range of 0.01–0.1 μg/kg/min has been described, although when used alone, we have found efficacy as high as 0.2 μg/kg/min. In Manninen and colleagues’ 2006 study, propofol infusion combined with intermittent fentanyl yielded similar patient satisfaction, recall, and intraoperative complications to remifentanil, with a slightly higher rate of respiratory depression in the propofol and fentanyl group. Emergence from remifentanil-propofol has been described as approximately 9 minutes. Sedation with remifentanil infusion alone is performed in some centers, although no data have been published at this time. Alfentanil is known to induce epileptiform discharges in the hippocampal area and should be used with caution in patients with complex partial epilepsy. For patient comfort, an opioid infusion may be continued at a low dose during testing, titrated to effective patient cooperation. Longer-acting analgesia may be necessary prior to emergence, although emergence on low-dose opioid infusion continued to recovery may be used.
The alpha-2-agonist dexmedetomidine also may be used and has been recommended, due to its lack of interference with electrophysiologic testing, sedation with minimal respiratory effects, , and anxiolytic and analgesic qualities. A loading dose of 1 μg/kg is delivered over 10–15 minutes with an infusion rate of 0.1–0.6 μg/kg/h. Doses are higher in children. Dexmedetomidine use as a lone sedating agent has been described, as well as a combined anesthetic with propofol or opioids, or both. The use of remifentanil combined with dexmedetomidine has also been reported. Like remifentanil, dexmedetomidine may be continued at low doses during brain mapping and functional testing if needed for patient comfort. Dexmedetomidine is known to have a significant synergistic effect when used in combination with other sedative agents.
Droperidol and fentanyl were commonly used in the past, but neuroleptanalgesia has given way to faster acting and more quickly eliminated regimens.
Brain Mapping and Cognitive Testing
As patients emerge from deep sedation or anesthesia, the anesthesiologist must take responsibility for safely re-orienting the patient, providing a calming influence, and guiding him or her through the brain mapping and cognitive testing phase. The use of bispectral-index monitoring to shorten emergence has been described and may be useful. The patient may be disoriented for a brief period after sedation. Again, preoperative preparation becomes essential during this phase. As the patient is guided through the process, he or she must be reassured that involuntary movements and speech patterns may occur as a result of cortical stimulation by the surgical team. The anesthesia team must be prepared to address any anxiety and discomfort that may occur. Motor, sensory, cognitive, and speech testing may be performed during this time. The patient may be asked to verbally identify objects or pictures, read passages aloud, perform specific motor tasks, or identify paresthesias or other sensations. Cortical evoked potentials and electrocorticography (ECoG) may be used to identify functional tissue and seizure foci. The results of this testing will guide the surgeon in removing pathologic tissue with minimal disruption to eloquent tissue in order to reduce patient morbidity. Surgical resection then proceeds while the patient completes verbal tasks (speech area assessment) or performs motor tasks (motor area assessment). Seizure activity is also possible during this phase, and the anesthesiologist must be prepared for prompt treatment, possible airway intervention, and conversion to general endotracheal anesthesia.
When brain mapping and functional testing are complete, the patient should be sedated once more for closure of the dura, calvarium, and scalp. This period can be very stimulating to the patient and adequate sedation can usually be achieved with remifentanil, propofol, dexmedetomidine, or a combination of these agents, as has been described.
Adverse Events and Management
Seizures, respiratory depression, nausea, vomiting, anxiety, discomfort, and agitation may occur during awake craniotomy. As is commonly the case with sedation, airway obstruction, hypercarbia, and hypoxemia are all possible, and careful preoperative assessment of the airway is vital. We have also experienced laryngospasm with LMA during the asleep portion of the asleep-awake-asleep technique. An extensive review of anesthetic complications of awake craniotomies showed an 18.4% rate of hypoxemic events for patients undergoing sedation for the procedure compared to merely 1% in patients who received endotracheal intubation. Airway or ventilation complications occurred in just 2% when patients received propofol- only sedation. The rate of conversion to general anesthesia has been reported to be 2%. Dexmedetomidine appears significantly better than propofol for rate of respiratory depression. Dexmedetomidine has been described for rescue of a patient unable to tolerate awake brain mapping after a propofol- remifentanil sedation regimen, and is now used more commonly as a primary sedative. Airway-assist maneuvers and the use of oral or nasal airways are common in patients undergoing sedation and should be expected to treat transient obstruction.
Vomiting and aspiration are possible in the sedated patient. As the airway will be unprotected using this technique, administration of prophylactic antiemetics is advisable, and rapid treatment should be provided if nausea occurs. The incidence of nausea and vomiting is 4% for mixed sedation techniques and even less for the use of propofol. Once symptoms occur, they can be controlled with a hydroxytryptamine-3 receptor (HT-3) antagonist, such as metoclopramide 10 mg. Nausea can also result from inadequate analgesia of dural attachments and meningeal vessels. Additional local anesthetic should be administered by the surgeon and supplemental sedation administered by anesthesia.
Sedation with spontaneous ventilation may pose the problem of brain swelling, particularly when mass-effect already exists, due to hypopnea or periods of apnea and concomitant increase in PaCO 2 . However, spontaneous ventilation also may assist in keeping the brain relaxed due to maintenance of negative intrathoracic pressure and promotion of cerebral venous outflow. Mannitol or furosemide administration may be necessary to reduce swelling and improve the surgical field. Patient movement—with the head in pins or during craniotomy— can have morbid outcomes, including scalp and soft tissue injury, brain swelling from straining, and placing the cervical spine at risk. It is critical to anticipate possible patient movement—during times like emergence from sedation or as a result of seizure initiated during mapping or delirium—and control the movement quickly. Deepening sedation with propofol boluses may be effective, and conversion to general anesthesia must be considered if necessary. It is important to be aware that deepening sedation may result in hypopnea or apnea, and the anesthetic team must be prepared to take control of the airway.
Seizures may occur from electrical stimulation during brain mapping or from a patient’s underlying condition. Vigilance is critical because the untreated seizure while in head pins could be catastrophic. Seizure activity can be treated with propofol (0.75–1.25 mg/kg) or benzodiazepines, depending on the need for subsequent electroencephalograph (EEG) recording. A 4.9% incidence of seizures was reported with cortical mapping in an unselected series of 610 awake craniotomies. At the end of the procedure, benzodiazepines and phenytoin may also be used more freely.
Epilepsy surgery
Epilepsy is a disease of the brain characterized by: two unprovoked seizures greater than 24 hours apart; one unprovoked seizure; and a probability of seizures similar to the general recurrence risk after two unprovoked seizures occurring over the next 10 years, or diagnosis of an epilepsy syndrome. It is present in 0.5–2.2% of the general population. Because 30–40% of epileptics do not respond adequately to pharmacologic intervention, more than 400,000 people still have medically uncontrolled epilepsy in the United States. However, only 10–30% of patients with seizures refractory to medical management are appropriate candidates for seizure surgery, and only 1% eventually undergo the procedure.
Epilepsy is classified as partial, generalized, or psychogenic nonepileptiform seizures (PNES). Partial seizures are characterized by electrical disturbances localized to one area of one cerebral hemisphere. Simple partial seizures are not associated with a loss of consciousness, and generally last 1 minute or less. Complex partial seizures are characterized by a loss of consciousness or awareness and spread from their localized focus to other regions. Complex partial seizures may spread to become generalized. Generalized seizures have no demonstrated focal onset, although they may evolve from focal seizures, affect both hemispheres of the brain, and are characterized by a loss of consciousness. They are sub-categorized as generalized tonic-clonic (grand mal), tonic, myoclonic, absence (petit mal), and atonic. PNES are psychogenic episodes that may be characterized by seizure-like physical manifestations but have no corresponding epileptiform activity on EEG and are considered conversion reactions.
Surgical management of epilepsy may be an option for patients with intractable epilepsy refractory to medical treatment. With successful surgical intervention, lifestyle improves, although most patients continue anticonvulsant therapy. Chin et al. reported that the rate of employment improved only modestly in their group of 375 patients, from 39.5% fully employed status preoperatively to 42.8% postoperatively; however, the rate of part-time employment nearly doubled, from 6.9 to 12.4%.
Anesthetic regimens have a significant effect on cortical mapping for epilepsy and may reduce or improve the effectiveness of testing and surgery. While many anesthetic agents have anticonvulsant properties, many also have varying profiles of proconvulsant or pharmacoactivating properties that can be useful in intraoperative localization of epileptogenic foci. Alternately, other agents may confound ECoG testing and lead to poor localization and less effective outcomes. Pharmacologic interactions between anticonvulsant medications and anesthetic drugs must also be taken into account. Pharmacoactivation of interictal epileptiform activities (IEAs) can be necessary in patients who do not demonstrate spontaneous interictal discharges during ECoG. The goals of the anesthetic regimen should be discussed with the neurosurgeon, neurologist, or neurophysiologist to determine if pharmacoactivation will be required. This may change during the procedure if the patient fails to generate IEAs spontaneously or under electrical stimulation. A goal-oriented anesthetic plan in concert with the neurosurgical team and knowledge of the activating properties of various anesthetic agents are essential.
Pharmacology of Anesthetic Agents
Proper sedation can be achieved through the use of a variety of anesthetic plans. In many cases, a general endotracheal anesthetic is preferred. In others, an awake craniotomy is performed for better functional testing and identification of seizure activity. Visualization of seizure activity that is similar to the patient’s typical seizures can be very helpful in identifying the true epileptogenic focus. Iatrogenic activation of IEAs may be achieved with administration of proconvulsant anesthetics and awareness of their anticonvulsant activities. EEG recordings support altering the activation and inhibition of the cerebral cortex with administration of anesthetic agents. For example, during light sedation, cortical activation with higher- frequency beta activity predominates, which progresses to slow-wave activity as sedative or anesthetic depth increases.
Sedative-Hypnotic Agents
As a group, sedative-hypnotic agents have the greatest variation and most confusing profile regarding effects on epileptogenic activity. Most agents can generate neuroexcitatory effects when used at low doses and neurodepressive effects when used at higher doses. Several induction agents, such as propofol and thiopental, can induce myoclonic movements not associated with EEG excitatory activity; whereas others, such as etomidate and methohexital, have been shown to generate both myoclonus and EEG-documented epileptiform activity in patients. , Motor stimulatory phenomena, such as myoclonus, opisthotonus, and tonic-clonic activity, may occur with varying frequency in both epileptic and nonepileptic patients during induction with these agents, but only a few agents actually produce cortical electrical activity suggestive of seizures.
Barbiturates and benzodiazepines have substantiated anti- convulsive properties and are recommended for treatment of refractory status epilepticus.
Propofol is among the most commonly used induction and maintenance agents in general anesthesia for epilepsy surgery and awake craniotomy. Propofol has been shown to depress ECoG recordings, decrease the frequency of spike activity, and produce a minimal effect on spontaneous IEAs. Propofol decreases the frequency of epileptogenic spikes and quiets existing seizure foci, particularly in the lateral and mesial temporal areas. One study demonstrated spike activation with low-dose propofol. There have been reported cases of tonic-clonic seizures with propofol, and myoclonic activity not related to excitatory EEG activity may be seen. Propofol may obscure spike wave activity for up to 20 minutes after termination of infusion and should be discontinued prior to ECoG testing.
Etomidate has been shown to activate EEG seizure activity at induction doses in patients with a history of epilepsy and may also generate myoclonic activity. It has been shown to have a high activation rate and demonstrates successful spike activation during intracranial electrode testing. At higher doses, etomidate may produce burst suppression and break status epilepticus. , To date, its use in intraoperative ECoG has not been studied.
Methohexital has been shown to activate EEG seizure activity in patients with epilepsy and may assist with activation of ictal foci during ECoG. It is associated with a high percentage of spike activation (50–85%), although with questionable specificity, showing up to 43% inappropriate activation in one study.
Dexmedetomidine may be a favorable agent for awake craniotomy due to its effects of sedation, analgesia, and anxiolysis; the absence of motor stimulatory effects; and the lack of respiratory depression. Dexmedetomidine does not affect background ECoG activity or IEAs and may be the best alternative for awake craniotomy. , ,
Ketamine may induce nonspecific activation of IEAs, especially in the limbic structure, and can activate seizure activity in patients with epilepsy. , It has been used to assist with activation of ictal foci during intraoperative ECoG. Ketamine appears to have a dose-dependent threshold for seizure generation, with most reported cases of clinical seizure activity occurring when doses larger than 4 mg/kg are administered. ,
Opioids
Synthetic opioids such as alfentanil, fentanyl, sufentanil, and remifentanil are commonly used in neurosurgical anesthesia because of their short duration of action and their ability to minimize cortical effects through continuous infusion. High doses of synthetic opioids have proepileptic properties. Standard maintenance doses of these agents do not significantly increase the risk of perioperative seizures or effects on ECoG. However, bolus doses of synthetic opioids, such as alfentanil and remifentanil, increase spike wave activity in the interictal foci of patients undergoing intraoperative ECoG. , Due to their high effectiveness and specificity, bolus doses of these agents are used to facilitate location of the ictal cortex through stimulation of spike wave phenomenon with concomitant depression of background EEG. Alfentanil has been shown to be the most effective and specific synthetic opioid for pharmacoactivation. Fentanyl has been associated with epileptiform electrical activity in subcortical nonictal cortical tissue and has been shown to be associated with contralateral activity. The clinical history of the use of synthetic opioids in large numbers of epileptic patients undergoing ablative procedures suggests that synthetic opioids can be used safely in this patient population without a significant increase in the risk of perioperative seizures. Morphine and hydromorphone used at clinically relevant doses do not appear to have significant proconvulsant activity.
Volatile Inhalational Agents and Nitrous Oxide
The epileptogenic potential of isoflurane, desflurane, and halothane appears low, and there have been no reported seizures when used in isolation. However, there are rare reports of myoclonic activity with a normal EEG. Convulsions with spike and wave activity on EEG have been reported with combinations of isoflurane and nitrous oxide (N 2 O). , Although N 2 O has been associated with seizure generation when used to supplement other agents, it appears to be fairly inert in both the development and the treatment of seizure activity in humans. Both N 2 O and isoflurane have been used for many years at multiple institutions with a good safety record in epileptic patients.
Enflurane, used with or without N 2 O, has been the most common offender, with reports of intraoperative and postoperative myoclonus and EEG-demonstrated epileptiform activity in both epileptic and nonepileptic patient populations. , , , , The incidence of EEG spike wave production with enflurane appears to be dose dependent. The end-tidal concentration that triggers maximum epileptiform activity is reduced during hypocapnia. Enflurane has fallen out of favor as new inhalational agents have become available, and it is now rarely used clinically in the United States. Enflurane should be avoided in patients with epilepsy unless the desired effect is to trigger seizures during ECoG.
Sevoflurane (not desflurane) has been reported to generate convulsions as well as electrical spike waves in both epileptic and nonepileptic patients. , The frequency of spike wave activity with sevoflurane increases with dose escalation and hyperventilation ( Fig. 17.2 ). , Hisada and colleagues reported that widespread neuroexcitatory activity associated with sevoflurane did not facilitate seizure focus localization in patients with temporal lobe epilepsy. Hyperventilation decreases the prediction specificity of leads with ictal spikes and should be employed cautiously during ECoG.
Muscle Relaxants
Long-term anticonvulsant therapy with phenytoin, carbamazepine, or both, is associated with resistance to the effect of nondepolarizing neuromuscular blockers, including pancuronium, vecuronium, metocurine, cisatracurium, and rocuronium, but less so with atracurium. , The etiology of this phenomenon is likely both pharmacodynamic and pharmacokinetic. ,
Anesthetic Management
Goals
Preoperative assessment of the patient’s neurologic condition, as well as comorbidities, is essential. Careful attention should be paid to anti-seizure medications. Intraoperative goals include maintenance of appropriate cerebral blood flood and perfusion, control of brain bulk, and rapid emergence from anesthesia for postoperative neurologic evaluation. In the event that seizure induction is desired, the goals of the anesthesiologist include selection of effective inducing agents and avoidance of patient injury. Careful postoperative monitoring of the patient’s neurologic status is required, and postoperative seizure control may be necessary.
Preoperative Evaluation
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