Cognitive aids and evidence-based checklists are frequently utilized in complex situations across many disciplines and sectors. The purpose of such aids is not simply to provide instruction so as to fulfill a task, but rather to ensure that all contingencies related to the emergency are considered and accounted for and that the task at hand is completed fully, despite possible distractions. Furthermore, utilization of a checklist enhances communication to all team members by allowing all stakeholders to know and understand exactly what is occurring, what has been accomplished, and what remains to be done. Most clinicians are already quite familiar with checklists and algorithms in the routine care of their patients and in preparation for invasive procedures, often in the form of “timeouts,” and for crisis management, such as adherence to the American Heart Association Advanced Cardiac Life Support (ACLS) guidelines.1 In recent years Ariadne Lab2 and the Stanford Anesthesia Cognitive Aide Group3 have developed guides for common adult anesthetic emergencies. The Society for Pediatric Anesthesia developed and published cognitive guides for pediatric patients in 2014.4
The Society for Neuroscience in Anesthesiology and Critical Care (SNACC) Education Committee has developed a set of evidence-based critical event cognitive aids for neuroanesthesia emergencies. The committee is comprised of an international group of neuroanesthesiologists, neurocritical care intensivists, and neuroscientists. These cognitive aids were designed to provide an expert consensus for the management of neuroanesthetic emergencies based on current literature. While these cognitive aids are designed to be available and easily accessible in an online format for the purposes of treating an emergency in the perioperative environment, this manuscript introduces these guides in a text format and provides a summary of the current diagnostic and therapeutic literature for each emergency event. All members of SNACC had the opportunity to review and comment on a draft of this document and the cognitive aids. Their feedback was incorporated into the final product which was subsequently reviewed and agreed by the SNACC Executive Committee before publication.
Each cognitive aid is designed to be a quick reference for clinicians facing a neuroanesthetic emergency. Each card or guide has a standard layout to improve the ease of information finding, and begins with a brief description of the clinical signs and symptoms of said emergency. Initial steps to stabilize the patient, common medications, next steps in treatment, differential diagnosis, and common causes are included in individual tables within each guide. An example of a cognitive aid card (for the management of cerebral vasospasm) is shown in the relevant section below, and all are available in the supplementary material (Supplemental Digital Content Fig. 1, Supplemental Digital Content 1, https://links.lww.com/JNA/A80).
The neuroanesthetic events or emergencies which are addressed in these cognitive aids include: acute stroke, intraoperative aneurysm rupture (operating room and neurointerventional radiology suite), autonomic hyperreflexia (AH) after spinal cord injury (SCI), major bleeding during spine surgery, delayed emergence after craniotomy, intraoperative management of raised intracranial pressure (ICP), loss of neuromonitoring evoked potentials, seizure during craniotomy, cerebral vasospasm, and venous air embolism (VAE).
ACUTE ISCHEMIC STROKE
Stroke is the third leading cause of death in developed countries and the leading cause of long-term disability worldwide.5 The World Health Organization defines the person sustaining a stroke as having “rapidly developed signs of focal (or global) disturbance of cerebral function lasting longer than 24 hours (unless interrupted by death) with no apparent cause other than of vascular origin.”6 Patients usually present with altered mental status, hemiparesis, visual loss, dysarthria, facial drop, vertigo, or ataxia.
Ischemic strokes are much more common than hemorrhagic strokes, accounting for 85% to 95% of all stroke cases. Brain imaging is essential to differentiate between the 2 etiologies. It is of vital importance to minimize the time between onset of symptoms (ie, last time seen normal) and treatment initiation after ischemic stroke. Because of this, initial evaluation must be performed as quickly as possible. Active treatment options may include either intravenous thrombolysis with recombinant tissue plasminogen activator or neuroendovascular interventions. The former is indicated within 3 hours of the onset of symptoms, but multiple contraindications exist, including blood pressure >185/110. Neuroendovascular interventions include intra-arterial thrombolysis or mechanical clot extraction, and they can be indicated for patient with major stroke caused by large vessel occlusion within 6 hours of symptoms onset.7
The decision regarding type of anesthesia (general anesthesia or conscious sedation) for the endovascular intervention should take into consideration multiple factors. Previously, a meta-analysis of 9 retrospective studies suggested that general anesthesia was associated with worse functional outcomes and higher mortality rates.8 Because of the retrospective nature of these studies, it was thought that this association could have been biased by the fact that patients with worse clinical state and poorer prognosis were selected to undergo the procedure under general anesthesia. Recently, 3 prospective randomized controlled trials (GOLIATH, AnStoke, and SIESTA) compared the use of general anesthesia versus conscious sedation for endovascular stroke treatment.9–11 They did not demonstrate any difference in neurological outcomes between the 2 anesthesia types, and found no delay in time to reperfusion in the general anesthesia group. General anesthesia was associated with higher rates of successful reperfusion. In contrast, conscious sedation was associated with worse angiographic quality and more frequent patient movement. Intraprocedural decrease in mean arterial pressure >40% was an independent predictor for poor neurological outcome. Hence, regardless of anesthesia technique, a strict protocol for aggressive management of intraprocedural systemic blood pressure should be adopted during endovascular stroke treatment.
Intraoperative anesthetic management aims to maintain adequate perfusion to the brain. Anesthetic goals should include: (1) tight control of blood pressure, preferentially with continuous invasive monitoring and a blood pressure goal of >140/90 mm Hg; (2) oxygen supplementation to maintain hemoglobin saturation (SpO2) >92%; (3) maintenance of eucapnia to avoid cerebral vasoconstriction (end-tidal carbon dioxide concentration 35 to 45 mm Hg); (4) temperature maintained between 35 and 37°C; and (5) monitoring of blood glucose at least every hour and maintenance of euglycemia (70 to 140 mg/dL).
INTRAOPERATIVE ANEURYSM RUPTURE
In the United States, the incidence of aneurysmal subarachnoid hemorrhage (SAH) is reportedly between 10 and 15 people per 100,000 population.12,13 Lower rates (2 to 4 per 100,000) are reported in China and Central America, while Finland and Japan note slightly higher rates (19 to 23 per 100,000).14
The only effective method of preventing primary rupture or rebleed of an intracranial aneurysm is definitive treatment of the aneurysm. Intraoperative/intraprocedural aneurysm rupture (IAR) is the most devastating concern in both unruptured and ruptured aneurysm repairs, although patients with aneurysmal SAH are also at high risk for periprocedural cardiac, neurological, and pulmonary complications.
Although no large scale studies have evaluated the incidence of IAR during clipping or coiling, several case series have found varying rates ranging from 7.6% to 34.9% for clipping and 2% to 4.5% for coiling. Similarly, the reported mortality and neurological disability rates secondary to IAR are highly variable, ranging from 0% to 40% with endovascular coiling and 0% to 33% with surgical clipping.15 These numbers suggest that efforts to understand risk factors and optimize intraoperative management of IAR are warranted. The timing of IAR can be categorized as either preaneurysm exposure or postexposure. IAR may occur during any phase of the procedure, but is associated with a higher mortality rate when it occurs before the aneurysm is exposed.16 Anesthetic and hemodynamic management of IAR varies somewhat with the timing of rupture.
Aneurysmal rupture occurring during induction of anesthesia although rare is associated with increased morbidity. In the event of preexposure IAR, steps to decrease ICP and improve surgical exposure should be undertaken. Steps should be taken to increase cerebral venous drainage by elevating the head as allowed, maintaining the head in a neutral position as possible, and decreasing any obstruction to venous outflow (eg, loosening cervical collar, noncircumferential securing of endotracheal tube). Cerebral perfusion pressure (CPP), oxygenation and ventilation should be optimized. Care should be taken to maintain the transmural pressure gradient (TMPG) as either an increase or decrease can result in IAR.17 Excessive hyperventilation should be avoided as this can decrease ICP dramatically and dangerously elevate the TMPG. ICP should also be controlled so as to maintain an appropriate TMPG, that is an external ventricular drain (EVD) should not be opened as this can worsen bleeding from the aneurysm. Osmotherapy can be administered to decrease brain edema (eg, mannitol 0.25 to 1 g/kg or 3% hypertonic saline with a sodium goal of 145 to 155 mEq/L).
In the event of postexposure IAR, induced hypotension (mean arterial pressure 50 to 60 mm Hg) can be used to decrease bleeding and improve surgical visualization. Consider temporary flow arrest to facilitate clipping with adenosine (0.3 to 0.4 mg/kg) which is capable of providing a brief period of profound systemic hypotension with low perioperative morbidity.18 Maneuvers to decrease cerebral metabolic rate of oxygen consumption through burst-suppression should be taken (eg, propofol bolus 50 to 100 mg and infusion to >125 mcg/kg/min). Patients should undergo volume resuscitation after clip placement with isotonic intravenous fluid and/or red blood cells (goal hemoglobin >8 g/dL). Patients treated with anticoagulant or antiplatelet therapy may require reversal of these therapies if IAR occurs.
Aneurysm rupture is also a possible complication during endovascular coiling in the neurointerventional radiology suite. Signs of rupture in this setting might include extravasation of contrast on radiologic imaging, and/or sudden hypertension and bradycardia due to increased ICP. Treatment unique to IAR during endovascular coiling includes consideration of the need for urgent reversal of anticoagulation. If heparin has been administered during the procedure, emergent reversal with protamine, in close communication with the proceduralist and dosed according to the most recently measured activated clotting time, is usually indicated. As with aneurysm rupture which might occur before or during open clipping, blood pressure should be tightly controlled and elevated ICP treated acutely. CPP should be maintained while at the same time avoiding systemic hypertension which might contribute to worsening of the vascular leak. Neurosurgery should be consulted for possible placement of an EVD and for potential emergent transfer to the operating room for hematoma evacuation and aneurysm clipping if hemostasis cannot be achieved in the interventional suite. Other temporizing measures must be taken in the meantime, including hyperventilation, administration of mannitol or hypertonic saline, initiation of burst-suppression, and elevation of the head as feasible. Finally, the availability of type and cross-matched blood should be confirmed.
In summary, IAR is a dreaded consequence of surgical clipping or endovascular coiling procedures in patients with previously ruptured or unruptured cerebral aneurysms. The risk of rupture is increased in patients with coronary artery disease, chronic obstructive pulmonary disease, hyperlipidemia, and those who experience hemodynamic lability, and may occur regardless of surgeon/interventionalist experience. The anesthetic management of aneurysm patients is a dynamic process that centers on blood pressure control as a means of maintaining adequate CPP and stabilizing the TMPG. The anesthesiologist must anticipate the steps of surgery or endovascular procedure and preemptively mitigate large hemodynamic swings that can occur at various stages of the procedure, as these abrupt changes increase the risk of aneurysmal rupture. In the event of IAR, clear communication with the operator is key, as is a systematic approach to hemodynamic control and volume resuscitation. If IAR does occur, the potential for hemodynamic instability secondary to massive hemorrhage necessitates early calls for assistance.
AH AFTER SCI
AH can be a life-threatening complication after SCI. It is defined as a blood pressure increase 20 mm Hg above baseline; however, it can manifest as a hypertensive crisis with severe complications.19 The prevalence of AH is ∼90% in patients with injuries at level T6 or higher.20 It can appear as soon as 2 to 3 weeks after the initial injury and usually presents within one year in affected individuals.
The etiology of AH is disruption of the descending inhibitory pathways to the sympathetic preganglionic neurons of the splanchnic vasculature. When a stimulus below the injury occurs there is widespread uninhibited vasoconstriction of this vasculature, leading to severe hypertension.19 Common causes include distension of the bowel or bladder, urinary tract infections, pressure ulcers, uterine contractions, and surgical stimulus.
Prevention of a triggering stimulus is paramount to avoiding the sequelae of AH. Therefore, adequate anesthesia, either via general or a regional technique, must be established before any procedure commences. Spinal anesthesia may be superior to epidural for reliable blockade and prevention of AH, as there are case reports of AH under epidural anesthesia.21 While determining the level and density of the block may be difficult in SCI patients, regional anesthesia remains an acceptable alternative to general anesthesia.
Signs of AH are related to the sympathetic surge, the hallmark of which is hypertension. These hypertensive episodes can quickly escalate into life-threatening situations with reflex bradycardia in many cases, given the preserved baroreceptor reflex. However, tachycardia and other dysrhythmias can also be observed. Sweating and flushing of the skin above the level of injury is common during episodes. Patients may also report a headache and/or nasal congestion. It is important to screen SCI patients for a history of AH, inciting stimuli, and resulting signs and symptoms.
Eliminating the offending stimulus and deepening the anesthetic, often times to >1 minimum alveolar concentration, is imperative.22 Potent direct vasodilating antihypertensive agents with rapid onset of action, such as nitroglycerin, nicardipine or nitroprusside, are the first-line treatment. To allow for precise titration of medication and monitoring of blood pressure, intra-arterial catheterization should be considered if the hypertensive episode is severe and does not dissipate quickly. If possible, the patient should be sat upright or the head of the bed elevated to allow orthostasis to further lower the blood pressure.
The patient who experiences a severe episode of AH should be monitored for signs of cerebral edema, myocardial ischemia, hemorrhage, seizures, pulmonary edema, and heart block. The most common serious outcome of AH is cerebral hemorrhage.23
MAJOR BLEEDING DURING SPINE SURGERY
The prevalence of spine surgery has been growing significantly over the last 2 decades, resulting not only in an increased number of surgeries per year but also in ever more complex procedures. The duration and complexity of these surgeries may result in significant bleeding and thus increased transfusion requirements, which are associated with negative patient outcomes, including longer hospital stays and increased overall cost.24–26 The rate of perioperative blood transfusion is considered a major outcome determinant, which has led to efforts to reduce transfusion requirements.27
Uncontrolled hemorrhage during spine procedures can be life-threatening, and exposure to blood products carries risks of potential complications.28,29 Strategies to reduce intraoperative blood loss begin with a careful preoperative evaluation to identify those at risk. The Prediction Model of Transfusion in Spine Surgery (PMTSS) is the first quantitative tool that predicts the need for blood transfusion in thoracolumbar spinal fusion surgery. The variables considered independent risk factors for blood loss are: age older than 50 years, preoperative anemia, multilevel spine surgeries, and osteotomy components to the procedure. A PMTSS score of >2 is highly predictive for transfusion of at least 1 unit of packed red blood cells during the perioperative period, which includes the period up to 5 days after surgery.30
Preoperative screening for anemia and coagulopathy is recommended at least 4 weeks before an elective case.31 The treatment of anemia is aimed at increasing the red blood cell mass,29 given that the risk of bleeding decreases when the preoperative hemoglobin level is close to the normal range.32 In addition to conventional coagulation studies, the use of thromboelastometry is now encouraged even in the preoperative setting as it measures the actual interaction of platelets and the coagulation cascade, thus enabling a more targeted treatment of coagulation deficiencies. This technology has been shown to reduce the risk of perioperative blood loss and has demonstrated reliability in predicting the need for massive transfusion.33
Careful patient preparation is of paramount importance. Ensuring adequate vascular access and confirming availability of blood products are mandatory steps before skin incision. Patient position is a major contributor to blood loss, as high intra-abdominal pressures are transmitted to the valveless epidural venous plexus, causing blood to ooze from osseous structures. Correlation between vertebral interosseous pressure and blood loss has been described, while the amount of bleeding appears to be less correlated with systemic arterial pressure.34 Accordingly, controlled hypotensive techniques have greatly fallen out of favor, and care should rather be taken to ensure that visceral organs are free of compression in the prone position.35
Tranexamic acid (TXA) is now routinely used in many centers during complex spine procedures due to its proven efficacy and apparently low side-effect profile. Dosing of TXA is not standardized and varies considerably between institutions, ranging from low dose regimens, 10 mg/kg bolus followed by 1 mg/kg/h infusion,36 to regimens with higher doses up to 30 to 100 mg/kg bolus followed by infusions of 1 to 10 mg/kg/h until wound closure.37–39 Aminocaproic acid is another antifibrinolytic agent that can be administered. However, its higher cost and the fact that it is not superior to TXA in reducing blood loss make TXA more favorable in most situations.39,40 TXA is known to increase the rate of atrial fibrillation, renal failure, and seizures in cardiac patients. Studies in orthopedic surgeries have found no increase in the incidence of TXA-related adverse effects such as thromboembolism.41,42
Close communication and cooperation between anesthesia and surgery teams is crucial when considerable bleeding is encountered. The management goal during massive hemorrhage is to achieve hemostasis as quickly as possible while maintaining adequate tissue perfusion. Active external warming devices should be utilized to ensure normothermia for optimal platelet function. It is debatable whether the routine use of autologous transfusion techniques is beneficial.43–45 However, according to the American Association of Blood Banks, cell salvage is indicated when blood loss exceeds 20% of estimated total blood volume or when no cross-matched blood products are available.43 Finally, in situations in which there is continuous blood loss and increasing transfusion requirements, temporary wound packing and staging of the procedure should be strongly considered.
Perioperative bleeding in spine surgery can have substantial impact on patient morbidity. Despite demonstrable benefits in various methods, no standardized protocol for blood conservation in spine surgery has been validated. Therefore, the authors suggest a combination of blood sparing techniques as a reasonable way to achieve both clinical benefit and cost-effectiveness. We also believe that prompt initiation of resuscitative measures will help control the bleeding, avoid allogeneic blood transfusion which in turn minimizes overall complications, and perhaps improve patient outcome after spine surgery.
DELAYED EMERGENCE AFTER CRANIOTOMY
Delayed emergence or lack of resumption of baseline mental status after craniotomy is particularly worrisome as it precludes the possibility for early postoperative neurological evaluation and may represent severe neurosurgical complications that necessitate prompt intervention. Criteria for delayed emergence should be justified based on preoperative mental status, anesthetics administered (type, dose, and timing), and neurosurgical expectations.
The first set of actions should include immediate correction of any cardiopulmonary instability, such as hypotension, hypoxia, and hypercapnia. Normothermia should also be ensured. Prompt notification of the surgical team for collaborative assessment should also occur. Further management should focus on ruling out any residual anesthetic effects,46–48 metabolic/endocrinological derangements,43,46,47 or neurosurgical complications.49–51
Significant residual anesthetic effects, including from volatile agents, opioids, neuromuscular blocking agents, benzodiazepines, barbiturates, propofol, ketamine, or lidocaine,47 will lead to delayed emergence.46–48 The anesthesiologist should check the dose and timing of administered anesthetic agents, the exhaled concentration of volatile agent, muscle twitches, presence of spontaneous breathing, and ventilation parameters to help determine if residual anesthetic effects are the cause of the delayed emergence. Excessive opioid effect can be reversed with incremental doses of naloxone, with the risk of reversal of the analgesic effect of the opioid considered. If residual benzodiazepine effect is thought to be contributory to the delayed emergence, incremental doses of flumazenil can be administered, however, weighed against the risk of seizure precipitation. Residual nondepolarizing neuromuscular blocking agents can be reversed with anticholinesterases or sugammadex (for rocuronium and vecuronium).52
Major metabolic or endocrinological derangements, such as hypoglycemia and hyperglycemia, hyponatremia, hypermagnesemia, severe acid-base disturbances, hyperammonemia, uremia, severe hypothyroidism, central anticholinergic syndrome, or drug intoxication also contribute to delayed emergence.46,47,53–55 Depending on the patient’s comorbidities and perioperative circumstances, arterial blood gas, drug screen, and other relevant laboratory tests should be performed in order to diagnose and treat any metabolic or endocrinological abnormalities.
Severe neurosurgical complications, such as cerebral ischemia and vascular occlusion, intracranial hemorrhage,49,50 elevated ICP, cerebral edema,51 hydrocephalus, a postictal state after intraoperative seizures, tension pneumocephalus, and surgical trauma, will delay emergence after craniotomy. Prompt diagnosis and management is paramount to patient outcome. Anesthesiologists must prepare for the need for emergent transport for computed tomography (CT) or magnetic resonance imaging, or for emergent angiography in the neuroradiology suite, and must collaborate with the neurosurgical team to ensure operating room availability for potential emergent surgical reexploration. If seizures or a postictal state are thought to be the cause of delayed emergence, electroencephalography (EEG) monitoring in the intensive care unit may be considered and antiepileptic drug therapy may be initiated.
INTRAOPERATIVE MANAGEMENT OF RAISED ICP
Raised ICP may complicate the surgical course and lead to deleterious perioperative consequences. Intraoperative management of raised ICP is crucial, and early aggressive interventions improve outcomes and reduce mortality.56,57 Subjective (eg, surgeon assessment of brain swelling), objective (eg, ICP and CPP measurement), and radiologic evidence of brain swelling are the most common indications to institute intraoperative ICP lowering treatment. Monitoring ICP provides an early prognostic indicator, especially for patients with severe traumatic brain injury (TBI).57
There are guidelines that identify threshold values of ICP and CPP indicating the need for surgical intervention,58 but there are no intraoperative thresholds for ICP and CPP described in the literature to guide non-surgical interventions. For TBI, critical thresholds of 14 mm Hg for ICP and 56 mm Hg for CPP have been proposed after hematoma evacuation, and ICP values of 20 mm Hg and CPP of 50 mm Hg for wound closure.57
Intraoperative goals for the management of raised ICP include: (1) maintenance of CPP, (2) monitoring and acute reduction of ICP (in TBI), (3) providing optimal surgical conditions, (4) avoiding secondary insults, (5) providing adequate analgesia and amnesia, (6) urgent assessment of adequate oxygenation/ventilation, and (7) hemodynamic support to maintain end organ perfusion.49 In terms of the maintenance of an adequate depth of anesthesia and analgesia, the choice of anesthetic agents includes: intravenous agents (thiopental, propofol, and etomidate), which will cause cerebral vasoconstriction due to flow-metabolism coupling and therefore cause a reduction of cerebral blood flow (CBF), cerebral blood volume, cerebral metabolic rate of oxygen, and ICP; volatile agents, on the other hand, should be administered at <1 minimum alveolar concentration, considering the minimal direct cerebral vasodilatory effects at this concentration. The use of sedatives to lower ICP does not improve outcome.57
Optimal positioning to improve cerebral venous drainage is critical, including neutral neck positioning and head elevation, with the understanding that this may be limited by necessities related to the surgical approach. The optimal head elevation can be titrated for each patient by means of transcranial Doppler ultrasonography or by measurement of jugular venous blood oxygen saturation. In addition this can be monitored by assessment of CPP.59
Medications that may be given to reduce raised ICP include: 20% mannitol (0.25 to 1.5 g/kg) as an intravenous bolus, being vigilant for renal, cardiac, or electrolyte disturbances; 3% hypertonic saline as a continuous infusion at 0.1 to 1 mL/kg/h, to target a serum sodium level of 145 to 155 mEq/L. The benefit of the use of furosemide alone or in combination with mannitol is unclear. Continuous hyperosmolar therapy is associated with improved survival, but is controversial in patients undergoing brain tumor surgery.60
Intraoperative drainage of cerebral spinal fluid via an EVD allows good control of ICP, especially during midline posterior fossa tumor surgeries. It also provides good emergency ICP reduction when tumor resection is not possible.61
Hyperventilation results in hypocapnia, leading to cerebral vasoconstriction. CBF is roughly linearly related to PaCO2 between 20 and 80 mm Hg.62 The CBF, cerebral blood volume, and ICP reducing effects of hypocapnia are apparent for <24 hours. This transient ICP reducing effect of hyperventilation is largely dependent on change in bicarbonate level (with lowering PaCO2) in cerebral spinal fluid which is rapidly stabilized by the brain through exchange of bicarbonate ions from extracellular fluid and normalization of pH levels. A typical goal PaCO2 value in the acute setting is 30 to 35 mm Hg; PaCO2 as revealed by arterial blood gas analysis, rather than end-tidal CO2, should be used to assess hypocapnia. The main complication associated with hyperventilation is a dangerous reduction in CBF, which can give rise to cerebral ischemia.63 Thus, the anesthesiologist must balance the benefit of brain relaxation against the risk of cerebral hypoperfusion.
There is a role for steroid administration in patients with tumors/vasogenic edema. Efficacy against tumor-related vasogenic edema is established, but there is no established benefit with cytotoxic edema associated with TBI or SCI.64
The treatment of seizures also plays an important role in lowering ICP.
Electrocorticographic (ECoG) monitoring can help in identification of epileptogenic foci. In patients with a history of epilepsy it is recommended that antiepileptic medications be administered in the perioperative setting. Anesthetic drugs that lower the seizure threshold should be avoided. Rapidly irrigating the surgical field with cold saline is also a helpful measure to halt acute intraoperative seizures.65
LOSS OF NEUROMONITORING EVOKED POTENTIALS
The use of intraoperative neurophysiologic monitoring (IONM) has become standard practice during spinal deformity surgery and routine during many other neurosurgical procedures.66,67 Surgical manipulation of the spine carries a risk of permanent morbidity to the patient. IONM provides the surgeon with real time feedback on the integrity of the neural tracts and can help identify injury to the spinal cord at a time when corrective measures can be taken to reverse the insult. Multimodal neuromonitoring consisting of somatosensory-evoked potentials (SSEPs), motor-evoked potentials (MEPs), and/or electromyography improves the sensitivity of IONM.66
Warning criteria for changes in MEPs and SSEPs should be agreed by the team; however, an amplitude reduction of >50% or >10% increase in latency for SSEPs and >50% to 80% decrease in amplitude for MEPs are commonly used thresholds.66–69
The first set of corrective actions should be aimed at the most likely etiology of the change in IONM. In cervical spine surgery, the steps associated with the highest risk of injury and therefore IONM changes are position, decompression, and fusion. If signals are lost during or shortly after positioning, repositioning the patient’s head is likely to improve signals.70 A sudden and complete loss of signal is more likely related to a technical issue, such as loss of an electrode, and the monitoring technician should evaluate for technical problems. Changes in anesthetic medications should also be considered, such as the administration of neuromuscular blockade, an intravenous bolus of medication, or an increase in volatile anesthetic concentration. In the event that the etiology of IONM change is not rapidly identifiable it is suggested that the first intervention be increasing mean arterial pressure.71
Further management of continued alterations in IONM can be divided into surgical, anesthetic, and physiological strategies. The surgical team should discuss and review operative interventions that occurred before the signal changes.66,72 Common causes of surgically related loss of IONM include distraction of the cord, screw misplacement, osteotomy, and/or passage of sublaminar wires. If an osteotomy was recently performed, consideration of in situ fusion and/or limitation of further correction should be considered.66
If the IONM change occurred in the absence of surgical manipulation, anesthetic and physiological changes should be explored and optimized. Common causes of anesthesia related change in IONM include a recently administered bolus of anesthetic medication or a change in volatile anesthetic concentration, leading to a change in the depth of anesthesia.66,71 Patients receiving volatile anesthetics might benefit from decreasing the concentration of the agent or converting to total intravenous anesthesia.71,72 Volatile anesthetics cause a dose dependent increase in latency and decrease in amplitude of SSEPs and MEPs, an effect that is potentiated by nitrous oxide.69
Alterations in several physiological parameters may also lead to changes in IONM, but hypotension, tachycardia, and hypothermia are frequent causes.66,72 The patient’s end-tidal CO2 and PaCO2 should be assessed and corrected to normal levels. Hypothermia to 35°C may also lead to alterations in evoked potentials. Further, regional hypothermia may lead to transient changes, which may be seen if the surgical team irrigates with cold saline.72 Anemia has been shown to lead to changes is SSEPs in animal models; however, human data are lacking.73
Regardless of the etiology for the change in IONM signals, the treatment is a team approach. Communication between surgical, anesthetic, and monitoring teams is paramount to patient outcome.
SEIZURE DURING CRANIOTOMY
Seizures may occur during craniotomy in patients with or without a previous history of seizures. Intraoperative seizures during awake craniotomy may present as a sudden loss of consciousness, fluttering eyelids, repetitive/rhythmic jerking movements of the head or limbs, stiffness, convulsions, or rapid brain swelling.74 If the patient is under general anesthesia (especially if a neuromuscular blocking agent is administered), characteristic EEG or ECoG changes may help identify the onset of seizures, although no overt clinical signs may be present.74
The patency of the airway and maintenance of adequate oxygenation and ventilation are the top priorities, especially during awake craniotomy. The anesthesiologist should immediately administer 100% oxygen and may need to perform bag-mask ventilation with an oral airway, or even place a supraglottic device.75,76 The surgeon should be notified to halt high-risk surgical manipulations and to administer ice-cold saline onto the cortical surface. Any cardiopulmonary instabilities (hypotension, hypoxia, etc.) or hyperthermia may contribute to the onset of seizures and necessitate prompt management.
If the seizure is short in duration and self-limited, surgery may proceed with caution. Patients should continue to receive continuous oxygen supplementation and be closely monitored for airway patency, oxygenation, ventilation, hemodynamics, and consciousness during awake craniotomy. If the seizure is not self-limited, the patient should be treated with incremental doses of propofol, midazolam, or barbiturate to terminate the seizure.76–78 A bite block should be placed to protect against traumatic oral injury during the seizure. If airway patency or oxygenation/ventilation is not maintained during awake craniotomy, a supraglottic airway or endotracheal tube should be placed. Video laryngoscopy or fiberoptic bronchoscopy may be considered to improve airway visualization during intubation since the patient’s head may be in a suboptimal position (for intubation) due to surgical need. The anesthesiologist should suction the patient’s oropharynx and consider placement of an orogastric tube to prevent pulmonary aspiration.
It is important to explore and address the underlying causes of the seizure. Metabolic derangements (hypoglycemia, hyponatremia, alkalemia/hyperventilation, severe hypocalcemia, hypomagnesemia, etc.), drug toxicity or withdrawal, and inadequate serum anticonvulsant levels may lead to seizures and need timely correction. Surgical insults, such as cortical stimulation, brain injury, cerebral hemorrhage, or ischemia, need to be addressed promptly.79,80 In addition, anesthetics with epileptogenic potentials should be discontinued and avoided.
Administration of antiepileptic drugs (eg, phenytoin, levitiracetam)76,77,81,82 and perioperative EEG monitoring should be discussed with the surgical team. The anesthesiologist should be prepared for the possibility of delayed emergence and the need for prolonged mechanical ventilation after surgery.
The differential diagnoses for changes in motor activity or behavior that resemble epileptic seizures during awake craniotomy include dystonia, shivering (hypothermia) nonepileptic seizures, anxiety spells, migraine headaches, and syncope.74,83,84 The former 2 may also be observed during craniotomy under general anesthesia in a patient who is not pharmacologically paralyzed. Characteristic EEG or ECoG changes will only be observed in epileptic seizures. It is important to distinguish epileptic seizures from nonepileptic behaviors, and thus ensure the delivery of appropriate treatment.
The critical event treatment guide for the management of cerebral vasospasm is shown in Figure 1.
Cerebral vasospasm in the purest sense is a radiologic diagnosis and is seen in up to 67% of patients who are imaged at the peak expected time of vasospasm after SAH.85 Of this number, 32.5% developed delayed cerebral ischemia (DCI), manifested as delayed neurologic deterioration. From a clinical standpoint, it is likely that symptomatology does not develop until there is about 50% luminal narrowing. Inherent to SAH is a global reduction in CBF with impairment of its usual auto regulation. Vasospasm thus represents a second regional ischemic insult in the perfusing territory of the affected vessel, and accounts for 10% to 50% of deaths after SAH in patients surviving the initial aneurysmal bleed.
Hemoglobin within red blood cells is spasmogenic and cerebral vasospasm is, hence, the result of the presence of blood within the subarachnoid space. The highest risk time for DCI is 3 to 14 days after SAH, with peak incidence at days 7 to 8.86 DCI may present with any constellation of the following symptoms: headache, neck stiffness, fever, confusion, a decline in mental status, or focal neurological deficits. Major risk factors include a larger amount of subarachnoid blood and poor clinical grade of the initial SAH. Other risk factors include age 40 to 59 years, history of hypertension, larger aneurysm size, intraventricular hemorrhage, hyperglycemia, smoking, and cocaine use. Of note, the prophylactic use of induced hypertension has been associated with an increased risk of vasospasm.87
In the consideration of the management of cerebral vasospasm, routine monitoring tools may be either diagnostic or serve as a trigger for definitive investigations. Clinical, radiographic, and physiological monitoring are essential for early detection as responsiveness to pharmacologic intervention decreases with time. The utility of clinical monitoring is less in patients with a larger initial insult.86
Physiological monitoring modalities include transcranial Doppler ultrasonography, EEG, brain tissue oxygen monitoring, cerebral microdialysis, thermal diffusion CBF monitoring, and near-infrared spectroscopy.86 Brain tissue oxygen monitoring directly measures tissue oxygenation and cerebral microdialysis the metabolic consequences of an imbalance between oxygen delivery and utilization, and changes in both may be predictive of infarction. Intracortical EEG may be superior to surface EEG in detection of DCI as may be evidenced by reduced alpha variability. Digital subtraction angiography (DSA) is the gold standard for diagnosis of cerebral vasospasm. CT angiography has shown good correlation with DSA but may overestimate the degree of vessel narrowing. CT perfusion has the added benefit of correlating the adequacy of blood flow for metabolic demand. DSA or CT angiography and perfusion combined is usually used for confirmation of cerebral vasospasm.86,87
While “Triple-H” therapy (hypertension, hypervolemia, and hemodilution) was previously recommended for the management for SAH, the current volume status goal is euvolemia. Hypertension independently improves CBF. Hypervolemia with consequent hemodilution also increases CBF but at the expense of blood oxygen content and by extension cerebral oxygen delivery. Despite this, a fluid bolus is reasonable at the start of management of vasospasm while initiating vasopressor therapy.87 The vasoactive medications most commonly employed to treat DCI are phenylephrine and norepinephrine. Dopamine is used to a lesser extent and vasopressin is considered a useful adjunct when very high doses of other vasopressors are required. Inotropes may be considered for inadequate response to induced hypertension. Blood pressure goals can either be a percentage increase (eg, 20%) above the starting blood pressure, or an absolute value. The target should be made based on the patient’s initial clinical response to blood pressure elevation. The presence of a second unruptured aneurysm does not contraindicate induced hypertension once the initially ruptured aneurysm has already been secured. In the presence of an unsecured aneurysm, judicious blood pressure elevation can be attempted.
Multiple randomized clinical trials have shown improved outcomes with the use of nimodipine after aneurysmal SAH, although not necessarily a reduction in the radiologic incidence of vasospasm.88 In addition, its effect is not a direct result of vasodilation.87 If nimodipine results in hypotension, a strategy of lower dose short interval dosing can be implemented, and, if this is ineffective, nimodipine can be discontinued. More invasive treatment options include angioplasty and intra-arterial vasodilator therapies, alone or in combination. Repeated treatments may be required.86 Nicardipine may also be utilized in patients where oral nimodipine is not feasible.89
The overall treatment goals, regardless of modality, are to optimize CBF, reduce cerebral metabolic rate, and avoid secondary injury.86 Prevention of this secondary injury also involves correction of hyponatremia, which is usually the result of cerebral salt wasting and is associated with ischemia. Management strategies should be aimed at avoiding hypovolemia, hypomagnesemia, hypotension, hyperglycemia, seizures, raised ICP, hypoxemia, and hypercapnia. It is also important to consider other significant differential diagnoses for the change in neurological state, including metabolic disturbances (eg, hyponatremia and hypernatremia), hypoxemia, hypercarbia, hypotension, hypovolemia, systemic infection, aneurysmal rebleed, hydrocephalus, meningitis, ventriculitis, and seizures with a postictal state.
Hemodynamically significant VAE is an uncommon but potentially fatal complication during surgery and anesthesia. It occurs when air or medical gas enters the venous system. The physiological response to VAE can be trivial or catastrophic depending on the volume and rapidity of air entrainment, location where the emboli lodge, and the patient’s general health status. Signs and symptoms of VAE can therefore vary significantly. However, oxygen desaturation, sudden reduction in end-tidal CO2, and hemodynamic instability are the classic presentations during general endotracheal anesthesia.90
Formation of VAE generally requires a negative pressure gradient and a communication between the vascular structures and the atmosphere. This classically happens in procedures where the level of the heart is below the surgical site (eg, sitting position craniotomy), creating a gravitational pressure gradient for air entry. It can also occur when noncompressible venous channels are breached, such as during spine surgeries or craniotomies involving dural venous sinuses. Other procedures at risk of VAE include laparoscopy, radiologic intervention, cesarean section, trauma, or even simple venous catheterization.91
Determination of the exact fatal volume of VAE is impossible to determine and is multifactorial. For instance, a small volume of air in coronary vessels can cause ischemia or significant arrhythmia leading to death, whereas a large amount of air slowly infused into the circulation can be gradually absorbed and cause no symptoms. Despite estimation of a lethal dose of air in humans at 3 to 5 mL/kg, it is recommended to be more conservative and consider a volume of <100 mL in adults as potentially fatal.92 The critical volume in children is certainly much less than in adults, and could be as low as 0.4 mL/kg in infants.93
Early detection of VAE helps decrease the severity of related complications. Transesophageal echocardiography provides the highest sensitivity in detecting as little as 0.02 mL/kg of air. However, its invasiveness, high cost, and the need for availability of equipment and personnel resources limit its use as a routine screening tool.90,91 Precordial Doppler monitoring is the most sensitive noninvasive method of detecting VAE but may be confounded by sound artifacts during concurrent use of electrocautery, and may be difficult or impossible to perform in the nonsupine or sitting position or when the patient is obese.91 Because of the lack of an ideal method, monitoring patients for VAE often requires close observation and a variety of modes of VAE detection.90,91
Serious consequences of VAE can be avoided or mitigated by initiating rescue steps quickly. The goals of management include reducing the volume of existing emboli, preventing further air entry, and hemodynamic support. Upon suspicion of VAE, a high fraction of oxygen (usually FiO2 1.0) is administered and nitrous oxide, if in use, stopped immediately. Aspiration of air from the right ventricle can be attempted if a central venous catheter (preferably multiorifice) is already in place. However, studies have shown that the volume of air removed is usually <20 mL. As the benefit of this maneuver is unclear, some anesthesiologist will not place a new catheter specifically for this indication unless other management options are exhausted, and the utility of this technique is controversial.94
Termination of air entrainment should be performed immediately while the above steps are taking place. Generally, the surgical team is asked to cover the operative field with saline or saline-soaked dressings so as to facilitate identification of the point of air entrainment. Bone wax may then be applied to seal the air entry point. Trendelenburg and left lateral decubitus positions place the right ventricular outflow tract below the right ventricle, causing the air to migrate into the right ventricle where it is less likely to cause an air-lock obstructing the pulmonary artery or to further embolize into the pulmonary circulation. However, repositioning may not be of benefit if right ventricular outflow tract obstruction is not present, and it precludes effective chest compression if needed, especially in the lateral decubitus position.95 The role of positive end expiratory pressure is controversial. To date, there is no strong evidence to suggest that it can prevent or stop air entrainment. Thus, positive end expiratory pressure should be used to improve oxygenation rather than as a means of minimizing the risk of VAE.91
In summary, hemodynamically significant VAE is an unlikely but potentially devastating complication during anesthesia and a variety of surgical procedures, including sitting craniotomy. The detection of VAE relies on vigilance of the anesthesiologist. Understanding the pathophysiology of this condition is very important and crucial in the development of the management strategies undertaken for prevention of the potentially catastrophic consequences of significant VAE.
Time is brain when handling acute neurosurgical and neuroanesthetic emergencies. The routine use of evidence-based checklists assists with an organized approach toward implementation of a stepwise algorithm for management of such emergencies, with the goal of better patient outcomes.
1. Neumar RW, Schuster M, Callaway CW, et al. 2015 American heart association guidelines update for cardiopulmonary resuscitation and emergency cardiovascular care. Circulation. 2015;132:S315–S367.
2. Ariadne Labs’ Operating Room Crisis Checklists. 2017. Available at: www.ariadnelabs.org
. Accessed May 17, 2018.
3. Stanford Anesthesia Cognitive Aide Group. Emergency manual, cognitive aides for perioperative critical events. 2016. Available at: www.emergencymanual.stanford.edu
. Accessed May 17, 2018.
4. Clebone A, Burian BK, Watkins SC, et al. The development and implementation of cognitive aids for critical events in pediatric anesthesia: The society for pediatric anesthesia critical events checklists. Anesth Analg. 2017;124:900–907.
5. Feigin VL, Lawes CM, Bennett DA, et al. Stroke epidemiology: a review of population-based studies of incidence, prevalence, and case-fatality in the late 10th century. Lancet Neurol. 2003;2:45–53.
6. The World Health Organization MONICA project (monitoring trends and determinants in cardiovascular disease): a major international collaboration. J Clin Epidemiol. 1988;41:105–114.
7. Talke OP, Sharma D, Heyer EJ, et al. Society for Neuroscience in Anesthesiology and Critical Care Expert Consensus Statement: anesthetic management of endovascular treatment for acute ischemic stroke. J Neurosurg Anesthesiol. 2014;26:95–108.
8. Brinjikji W, Murad MH, Rabinstein AA, et al. Conscious sedation versus general anesthesia during endovascular acute ischemic stroke treatment: a systematic review and meta-analysis. AJNR Am J Neuroradiol. 2015;36:529–529.
9. Simonsen CZ, Yoo AJ, Sørensen LH, et al. Effect of general anesthesia and conscious sedation during endovascular therapy on infarct growth and clinical outcomes in acute ischemic stroke: a randomized clinical trial. JAMA Neurol. 2018;75:470–477.
10. Lowhagen H, Rentzos A, Karlsson JE, et al. General anesthesia versus conscious sedation for endovascular treatment of acute ischemic stroke (The AnStroke Trial). Stroke. 2017;48:1601–1607.
11. Schonenberger S, Uhlmann L, Hacke W, et al. Effect of conscious sedation vs general anesthesia on early neurological improvement among patients with ischemic stroke undergoing endovascular thrombectomy: a randomized controlled trial. JAMA. 2016;316:1986–1996.
12. Labovitz DL, Halim AX, Brent B, et al. Subarachnoid hemorrhage incidence among Whites, Blacks and Caribbean Hispanics: the Northern Manhattan Study. Neuroepidemiology. 2006;26:147–150.
13. Shea AM, Reed SD, Curtis LH, et al. Characteristics of nontraumatic subarachnoid hemorrhage in the United States in 2003. Neurosurgery. 2007;61:1131–1137.
14. Ingall T, Asplund K, Mähönen M, et al. A multinational comparison of subarachnoid hemorrhage epidemiology in the WHO MONICA stroke study. Stroke. 2000;31:1054–1061.
15. de Rooij NK, Linn FH, van der Plas JA, et al. Incidence of subarachnoid haemorrhage: a systematic review with emphasis on region, age, gender and time trends. J Neurol Neurosurg Psychiatry. 2007;78:1365–1372.
16. Tummala RP, Chu RM, Madison MT, et al. Outcomes after aneurysm rupture during endovascular coil embolization. Neurosurgery. 2001;49:1059–1066; discussion 1066–1067.
17. Li MH, Gao BL, Fang C, et al. Prevention and management of intraprocedural rupture of intracranial aneurysm with detachable coils during embolization. Neuroradiology. 2006;48:907–915.
18. Bebawy JF, Gupta DK, Bendok BR, et al. Adenosine-induced flow arrest to facilitate intracranial aneurysm clip ligation: dose-response data and safety profile. Anesth Analg. 2010;110:1406–1411.
19. Phillips AA, Krassioukov AV. Contemporary cardiovascular concerns after spinal cord injury: mechanisms, maladaptations and management. J Neurotrauma. 2015;32:1927–1942.
20. Cragg J, Krassioukov A. Autonomic dysreflexia. CMAJ. 2012;184:66.
21. Schonwald G, Fish KJ, Perkash I. Cardiovascular complications during anesthesia in chronic spinal cord injured patients. Anesthesiology. 1981;55:550–558.
22. Yoo KY, Jeong CW, Kim SJ, et al. Sevoflurane concentrations required to block autonomic hyperreflexia during transurethral litholapaxy in patients with complete spinal cord injury. Anesthesiology. 2008;108:858–863.
23. Wan D, Krassioukov A. Life-threatening outcomes associated with autonomic dysreflexia: a clinical review. J Spin Cord Med. 2014;37:2–10.
24. Hughey AB, Lesniak MS, Ansari SA, et al. What will anesthesiologists be anesthetizing? Trends in neurosurgical procedure usage. Anesth Analg. 2010;110:1686–1697.
25. Ferraris VA, Davenport DL, Saha SP, et al. Surgical outcomes and transfusion of minimal amounts of blood in the operating room. Arch Surg. 2012;147:49–55.
26. Willner D, Spennati V, Stohl S, et al. Spine surgery and blood loss: systematic review of clinical evidence. Anesth Analg. 2016;123:1307–1315.
27. Carabini LM, Zeeni C, Moreland NC, et al. Development and validation of a generalizable model for predicting major transfusion during spine fusion surgery. J Neurosurg Anesthesiol. 2014;26:205–215.
28. Hu SS. Blood loss in adult spinal surgery. Eur Spine J. 2004;13 (suppl 1):S3–S5.
29. Theusinger OM, Spahn DR. Perioperative blood conservation strategies for major spine surgery. Best Pract Res Clin Anaesthesiol. 2016;30:41–52.
30. Lenoir B, Merckx P, Paugam-Burtz C, et al. Individual probability of allogeneic erythrocyte transfusion in elective spine surgery: the predictive model of transfusion in spine surgery. Anesthesiology. 2009;110:1050–1060.
31. Theusinger OM, Leyvraz PF, Schanz U, et al. Treatment of iron deficiency anemia in orthopedic surgery with intravenous iron: efficacy and limits: a prospective study. Anesthesiology. 2007;107:923–927.
32. Musallam KM, Tamim HM, Richards T, et al. Preoperative anaemia and postoperative outcomes in non-cardiac surgery: a retrospective cohort study. Lancet. 2011;378:1396–1407.
33. Naik BI, Pajewski TN, Bogdonoff DI, et al. Rotational thromboelastometry-guided blood product management in major spine surgery. J Neurosurg Spine. 2015;23:239–249.
34. Kakiuchi M. Intraoperative blood loss during cervical laminoplasty correlates with the vertebral intraosseous pressure. J Bone Joint Surg Br. 2002;84:518–520.
35. Lee TC, Yang LC, Chen HJ. Effect of patient position and hypotensive anesthesia on inferior vena caval pressure. Spine (Phila Pa 1976). 1998;23:941–947; discussion 947–948.
36. Elwatidy S, Jamjoom Z, Elgamal E, et al. Efficacy and safety of prophylactic large dose of tranexamic acid in spine surgery: a prospective, randomized, double-blind, placebo-controlled study. Spine (Phila Pa 1976). 2008;33:2577–2580.
37. Xie J, Lenke LG, Li T, et al. Preliminary investigation of high-dose tranexamic acid for controlling intraoperative blood loss in patients undergoing spine correction surgery. Spine J. 2015;15:647–654.
38. Dhawale AA, Shah SA, Sponseller PD, et al. Are antifibrinolytics helpful in decreasing blood loss and transfusions during spinal fusion surgery in children with cerebral palsy scoliosis? Spine (Phila Pa 1976). 2012;37:E549–E555.
39. Halanski MA, Cassidy JA, Hetzel S, et al. The efficacy of amicar versus tranexamic acid in pediatric spinal deformity surgery: a prospective, randomized, double-blinded pilot study. Spine Deform. 2014;2:191–197.
40. Louann M, Carabini NC, Moreland RJ, et al. A randomized controlled trial of low-dose tranexamic acid versus placebo to reduce red blood cell trasnfusion during complex multilevel spine fusion surgery. World Neurosurg. 2018;110:e572–e579.
41. Ho KM, Ismail H. Use of intravenous tranexamic acid to reduce allogeneic blood transfusion in total hip and knee arthroplasty: a meta-analysis. Anaesth Intensive Care. 2003;31:529–537.
42. Kushioka J, Yamashita T, Okuda S, et al. High-dose tranexamic acid reduces intraoperative and postoperative blood loss in posterior lumbar interbody fusion. J Neurosurg Spine. 2017;26:363–367.
43. Esper SA, Waters JH. Intra-operative cell salvage: a fresh look at the indications and contraindications. Blood Transfus. 2011;9:139–147.
44. Canan CE, Myers JA, Owens RK, et al. Blood salvage produces higher total blood product costs in single-level lumbar spine surgery. Spine (Phila Pa 1976). 2013;38:703–708.
45. Owens RK II, Crawford CH III, Djurasovic M, et al. Predictive factors for the use of autologous cell saver transfusion in lumbar spinal surgery. Spine (Phila Pa 1976). 2013;38:E217–E222.
46. Misal US, Joshi SA, Shaikh MM. Delayed recovery from anesthesia: a postgraduate educational review. Anesth Essays Res. 2016;10:164–172.
47. Tzabazis A, Miller C, Dobrow MF, et al. Delayed emergence after anesthesia. J Clin Anesth. 2015;27:353–360.
48. Douglas JH III, Ross JD, Bruce DL. Delayed awakening due to lidocaine overdose. J Clin Anesth. 1990;29:126–128.
49. Deuri A, Goswami D, Samplay M, et al. Nonawakening following general anaesthesia after ventriculo-peritoneal shunt surgery: an acute presentation of intracerebral haemorrhage. Indian J Anaesth. 2010;54:569–571.
50. Nakazawa K, Yamamoto M, Murai K, et al. Delayed emergence from anesthesia resulting from cerebellar hemorrhage during cervical spine surgery. Anesth Analg. 2005;100:1470–1471.
51. Kozasa Y, Takaseya H, Koga Y, et al. A case of delayed emergence from anesthesia caused by postoperative brain edema associated with unexpected cerebral venous sinus thrombosis. J Anesth. 2013;27:764–767.
52. Papathanas MR, Killian A. Sugammadex for neuromuscular blockade reversal. Adv Emerg Nurs J. 2017;39:248–257.
53. Razvi M, Bameshki A, Gilani MT. Delayed awakening from anesthesia following electrolyte and acid-base disorders, two cases. Patient Saf Qual Improv. 2014;2:65–68.
54. Garg R, Punj J, Pandey R, et al. Delayed recovery due to exaggerated acid, base and electrolyte imbalance in prolonged laparoscopic repair of diaphragmatic hernia. Saudi J Anaesth. 2011;5:79–81.
55. Mizuno J, Nakayama Y, Dohi T, et al. A case of hypothyroidism found by delayed awakening after the operation. Masui. 2000;49:305–308.
56. Stein SC, Georgoff P, Meghan S, et al. Relationship of aggressive monitoring and treatment to improved outcomes in severe traumatic brain injury. J Neurosurg. 2010;112:1105–1112.
57. Tsai TH, Huang TY, Kung SS, et al. Intraoperative intracranial pressure and cerebral perfusion pressure for predicting surgical outcome in severe traumatic brain injury. Kaohsiung J Med Sci. 2013;29:540–546.
58. Saul TG, Ducker TB. Effect of intracranial pressure monitoring and aggressive treatment on mortality in severe head injury. J Neurosurg. 1982;56:498–503.
59. Porchet F, Bruder N, Boulard G, et al. The effect of position on intracranial pressure. Ann Fr Anesth Reanim. 1998;17:149–156.
60. Asehnoune K, Lasocki S, Seguin P, et al. ATLANREA GroupCOBI Group. Association between continuous hyperosmolar therapy and survival in patients with traumatic brain injury—a multicentre prospective cohort study and systematic review. Crit Care. 2017;21:328.
61. Habib HAM. Intraoperative precautionary insertion of external ventricular drainage catheters in posterior fossa tumors presenting with hydrocephalus. Alexandria J Med. 2014;50:33–340.
62. Grubb RL Jr, Raichle ME, Eichling JO, et al. The effects of changes in PaCO2
on cerebral blood volume, blood flow, and vascular mean transit time. Stroke. 1974;5:630–639.
63. Coles JP, Fryer TD, Coleman MR, et al. Hyperventilation following head injury: Effect on ischemic burden and cerebral oxidative metabolism. Crit Care Med. 2007;35:568–578.
64. Hoshide R, Cheung V, Marshall L, et al. Do corticosteroids play a role in the management of traumatic brain injury? Surg Neurol Int. 2016;7:568–578.
65. Uribe A, Zuleta-Alarcon A, Kassem M, et al. Intraoperative seizures: anesthetic and antiepileptic drugs. Curr Pharm Des. 2017;23:6524–6532.
66. Bjerke BT, Zuchelli DM, Nemani VM, et al. Prognosis of significant intraoperative neurophysiologic monitoring events in severe spinal deformity. Spine Deform. 2017;5:117–123.
67. Thirumala PD, Crammond DJ, Loke YK, et al. Diagnostic accuracy of motor evoked potentials to detect neurological deficit during idiopathic scoliosis correction: a systematic review. J Neurosurg Spine. 2017;26:374–383.
68. Lall RR, Hauptman JS, Munoz C, et al. Intraoperative neurophysiological monitoring in spine surgery: indications, efficacy, and role of the preoperative checklist. Neurosurg Focus. 2012;33:E10.
69. Wang S, Zhang J, Tian Y, et al. Intraoperative motor evoked potential monitoring to patients with preoperative spinal deficits: judging its feasibility and analyzing the significance of rapid signal loss. Spine J. 2017;17:777–783.
70. Appel S, Korn A, Biron T, et al. Efficacy of head repositioning in restoration of electrophysiological signals during cervical spine procedures. J Clin Neurophysiol. 2017;34:174–178.
71. Yang J, Dkaggs DL, Chan P, et al. Raising mean arterial pressure alone restores 20% of intraoperative neuromonitoring losses. Spine. 2018;43:890–894.
72. Acharya S, Palukuri N, Gupta P, et al. Transcranial motor evoked potentials during spinal deformity corrections—safety, efficacy, limitations, and the role of a checklist. Front Surg. 2017;4:8.
73. Bithal RK. Anaesthetic considerations for evoked potential monitoring. J Neuroanaesthesiol Crit Care [serial online]. 2014;1:2–12.
74. Stafstrom CE, Carmant L. Seizures and epilepsy: an overview for neuroscientists. Cold Spring Harb Perspect Med. 2015;5:6.
75. Roppolo LP, Walters K. Airway management in neurological emergencies. Neurocrit Care. 2004;1:405–414.
76. Brophy GM, Bell R, Claassen J, et al. Neurocritical Care Society Status Epilepticus Guideline Writing Committee. Guidelines for the evaluation and management of status epilepticus. Neurocrit Care. 2012;17:3–23.
77. Erickson KM, Cole DJ. Anesthetic considerations for awake craniotomy for epilepsy and functional neurosurgery. Anesthesiol Clin. 2012;30:241–268.
78. Brevoord JC, Joosten KF, Arts WF, et al. Status epilepticus: clinical analysis of a treatment protocol based on midazolam and phenytoin. J Child Neurol. 2005;20:476–481.
79. Pouratian N, Reames DL, Frysinger R, et al. Comprehensive analysis of risk factors for seizures after deep brain stimulation surgery. Clinical article J Neurosurg. 2011;115:310–315.
80. Lowenstein DH. Current concepts: status epilepticus. N Engl J Med. 1998;338:970–976.
81. Swisher CB, Doreswamy M, Gingrich KJ, et al. Phenytoin, levetiracetam, and pregabalin in the acute management of refractory status epilepticus in patients with brain tumors. Neurocrit Care. 2011;16:109–113.
82. Beyenburg S, Reuber M, Maraite N. Intravenous levetiracetam for epileptic seizure emergencies in older people. Gerontology. 2009;55:27–31.
83. Lortie A. Psychogenic nonepileptic seizures. Handb Clin Neurol. 2013;112:875–879.
84. LaFrance WC Jr, Reuber M, Goldstein LH. Management of psychogenic nonepileptic seizures. Epilepsia. 2013;54 (suppl 1):53–67.
85. Dorsch NW, King MT. A review of cerebral vasospasm in aneurysmal subarachnoid haemorrhage Part I: incidence and effects. J Clin Neurosci. 1994;1:19–26.
86. Diringer MN, Bleck TP, Claude Hemphill J III, et al. Critical care management of patients following aneurysmal subarachnoid hemorrhage: recommendations from the Neurocritical Care Society’s Multidisciplinary Consensus Conference. Neurocrit Care. 2011;15:211–240.
87. Macdonald RL. Management of cerebral vasospasm. Neurosurg Rev. 2006;29:179–193.
88. Yong-fei L, Han-Cheng Q, Su J, et al. Drug treatment of cerebral vasospasm after subarachnoid hemorrhage following aneurysms. Chinese Neurosurg J. 2016;2:4.
89. Guilherme D, Noguiera R. Current options for the management of aneursymal subarachnoid hemorrhage-induced cerebral vasospasm: a comprehensive review of the literature. Interv Neurol. 2013;2:30–51.
90. Brull SJ, Prielipp RC. Vascular air embolism: a silent hazard to patient safety. J Crit Care. 2017;42:255–263.
91. Mirski MA, Lele AV, Fitzsimmons L, et al. Diagnosis and treatment of vascular air embolism. Anesthesiology. 2007;106:164–177.
92. Toung TJ, Rossberg MI, Hutchins GM. Volume of air in a lethal venous air embolism
. Anesthesiology. 2001;94:360–361.
93. Schwartz N, Eisenkraft JB. Probable venous air embolism
during epidural placement in an infant. Anesth Analg. 1993;76:1136–1138.
94. Martin RW, Ashleman B, Colley PS. Effects of cardiac output on the clearance of air emboli from the superior vena cava. Anesthesiology. 1984;60:580–586.
95. Muth CM, Shank ES. Gas embolism. N Engl J Med. 2000;342:476–482.