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 2 3 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 6
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 9–11
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 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 16
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
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
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 20
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
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
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
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 27
Uncontrolled hemorrhage during spine procedures can be life-threatening, and exposure to blood products carries risks of potential complications.28,29 30
Preoperative screening for anemia and coagulopathy is recommended at least 4 weeks before an elective case.31 29 32 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 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 37–39 39,40 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 43
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 43,46,47 49–51
Significant residual anesthetic effects, including from volatile agents, opioids, neuromuscular blocking agents, benzodiazepines, barbiturates, propofol, ketamine, or lidocaine,47 46–48 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
Severe neurosurgical complications, such as cerebral ischemia and vascular occlusion, intracranial hemorrhage,49,50 51
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 57
There are guidelines that identify threshold values of ICP and CPP indicating the need for surgical intervention,58 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 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 2 ) 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
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 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 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 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 71,72 69
Alterations in several physiological parameters may also lead to changes in IONM, but hypotension, tachycardia, and hypothermia are frequent causes.66,72 2 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 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 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
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
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
Administration of antiepileptic drugs (eg, phenytoin, levitiracetam)76,77,81,82
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
CEREBRAL VASOSPASM
The critical event treatment guide for the management of cerebral vasospasm is shown in Figure 1 .
FIGURE 1: Critical event treatment guide for the management of cerebral vasospasm. CT indicates computed tomography; TCD, transcranial Doppler.
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
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 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 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
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 87 86 89
The overall treatment goals, regardless of modality, are to optimize CBF, reduce cerebral metabolic rate, and avoid secondary injury.86
VAE
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 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 91 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 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.
CONCLUSIONS
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.
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