An Overview of Adult Acute Traumatic Neurologic Injury for the Anesthesiologist: What is Known, What is New, and Emerging Concepts

Abstract

Purpose of Review

We examine what is known, what is new, and what is emerging in acute neurotrauma relevant to the anesthesiologist.

Recent Findings

Timely and goal-directed care is critical for all patients requiring urgent/emergent anesthesia care. Anesthesia care for acute neurological injury should incorporate understanding the evolution of traumatic brain injury and spinal cord injury that translates to preoperative preparation, hemodynamic resuscitation, prevention of second insults, and safe transport between care settings. Anesthesia care should support optimizing patient outcomes.

Summary

Best practices involve extrapolating data from the intensive care unit setting since there is a lack of research addressing anesthesia care for acute neurological injury. There are opportunities to generate data to support evidence-based anesthetic care.

Introduction to Acute Neurotrauma

Neurotrauma, defined as traumatic injury to the brain and/or spine, is a global public health concern, primarily affecting lower-middle-income countries (LMIC) [1]. Approximately 49 million and 20.6 million people are annually affected by traumatic brain injury (TBI) and spinal cord injury (SCI) worldwide, respectively [1]; the primary cause is traffic accidents in lower-middle-income countries and falls in high-income countries [1, 2].

In the United States, there are approximately 214,000 TBI-related annual hospitalizations, 18,000 new SCIs yearly, and 305,000 people currently living with SCI [3]. Health disparities occur across the continuum of neurotrauma and acute care, including occurrence and limited access to care and rehabilitation [4]. The Centers for Disease Control and Prevention multistate TBI surveillance program [5] reports that every day in the United States, 586 (mostly elderly people) are hospitalized, and 190 (mostly elderly people) die from TBI [6]. TBI in adolescents and young adults contributes to 5.3 million Americans living with TBI-related disability. Major causes of TBI are falls, road traffic accidents, and firearms. Native Americans/Alaska Natives, who are 2.9% of the US population, experience the highest incidence of TBI-related hospitalization and death. African Americans, who are 12% of the US populace, experience the highest rate of homicide-related TBI deaths from firearms [7], highlighting racial and ethnic disparities in TBI occurrence and outcomes [8, 9]. Importantly, patients from marginalized groups with TBI are more likely to experience adverse long-term effects from TBI. Functional disability, psychiatric disorders, substance abuse, more injury, and likely a shortened life expectancy occur from inadequate access to suitable healthcare, follow-up, and rehabilitation. Economic instability, emotional disorders, and the burden of care negatively impact the families and communities already poorly positioned in a system of inequity that has historically denied them the benefits of a host of social determinants of health [10]. The relationship between federal research funding and outcomes only shows benefits for patients 55 years and older [11]. The recent National Academy of Science, Engineering, and Medicine’s Roadmap for Accelerating Progress makes important recommendations to improve TBI care, calling for transforming attitudes, understanding, investments, and healthcare systems that decrease unwanted variation in acute TBI care [12].

Early care of neurotrauma patients involves resuscitation, followed by urgent/emergent surgery and rehabilitation. In high-income countries, organized prehospital care systems initiate resuscitation and transfer to trauma centers. Anesthesiologists have unique expertise in acute care physiology, tracheal intubation, resuscitation, pain management, and critical care to prevent secondary injuries [13]. Knowing best practices and emerging concepts in acute neurological trauma is essential to all practicing anesthesiologists because patients with traumatic neurological injury often receive care in non-trauma centers. In addition, neurotrauma literature may not necessarily include guidelines or recommendations for intraoperative care and is primarily extrapolated from research in the intensive care unit or the emergency department. This review will discuss what is known, what is new, and emerging concepts in acute traumatic neurological injury that are relevant to perioperative care and present considerations for anesthesia management across trauma and non-trauma centers that are relevant to the perioperative care and Anesthesiology practice. Given the paucity of anesthesiology research in acute neurotrauma, there are no national-level guidelines for anesthesia care in acute neurotrauma. Hence, data from other clinical settings are used to guide anesthesiology care.

Methods

Human and Animal Rights

This study was not performed on human or animal subjects but is a synthesis of previously published research articles, some of which were performed by authors of this work.

Literature Search

We performed searches of EMBASE and PubMed databases from 2018 to 2023 and earlier for seminal work. Duplicates were removed, after which two authors reviewed each abstract for inclusion. Full-text primary research articles on TBI or SCI, applicable to anesthesia management and/or resuscitation, were included. Case reports, case series, animal studies, narrative reviews, and articles irrelevant to anesthetic management were excluded; search terms are given in Table 1. The PubMed search yielded 40 citations for TBI and 86 citations for SCI. EMBASE search yielded 281 citations for TBI and 193 citations for SCI. After removing duplicates, 294 and 254 citations screened TBI and SCI, respectively. Following the screening, 80 TBI and 59 SCI articles were identified for full review. Due to limited articles applicable to intraoperative care, literature or narrative review articles initially identified for abstract review were evaluated for references that might apply, producing 108 TBI articles for review After full review, author consensus, and editing, there were 64 TBI and 69 SCI articles (all within the last five years) included from the initial search. Given the paucity of intraoperative data identified from the first evaluation, the search was supplemented with additional published TBI articles in the last five years, identified by the author group, which results in additional 28 TBI articles. Finally, 161 (TBI: 92, tSCI: 69) were reviewed and included.

Table 1.

Search terms utilized within EMBASE and PubMed for evaluation of traumatic brain injury (TBI) and spinal cord injury (SCI) anesthesia literature

Subject	Search Terms
TBI	(‘traumatic brain injury’/exp OR ‘traumatic brain injury’ OR ‘pediatric traumatic brain injury’/exp OR ‘pediatric traumatic brain injury’ OR ‘traumatic brain injur*’:ti,ab,kw) AND (‘anesthesia’/exp OR ‘anesthesia’ OR ‘anesthesia’:ti,ab,kw OR ‘anaesthesia’:ti,ab,kw OR ‘anesthesiology’:ti,ab,kw) AND (‘perioperative period’/exp OR ‘resuscitation’:ti,ab,kw)
SCI	“Acute” AND (“Spinal cord trauma” OR “Spinal Cord Injury”) AND (“Anesthesia” OR “Anesthetic management” OR “Perioperative management” OR “Resuscitation” OR “Anesthesia Care”)

General Principles of Acute Trauma Care

The initial assessment of the traumatically injured patient begins with Advanced Trauma Life Support (ATLS) recommendations which begins with the primary survey (evaluation of Airway patency and Breathing adequacy followed by medication-assisted intubation as needed), Circulation assessment (with the establishment of intravenous access), and Disability assessment (neurological exam and Glasgow Coma Scale (GCS) score) and treatment/prevention of hypothermia [14]. Secondary and tertiary assessments involve identifying co-occurring injuries and final identification of injuries, as anesthesiologists, we will care of patients across this continuum.

Traumatic brain injury (TBI) is an alteration in brain function or other evidence of brain pathology caused by an external force [12] and TBI evolves after initial injury. Typically the assessment of TBI severity is made at admission but patients admitted to hospital with mild or moderate TBI may deteriorate. For patients with traumatic spinal cord injury (tSCI), due to its evolving nature, the assessment of spinal impairment (American Spinal Injury Association: ASIA) [15] is often performed towards the end of the first week after injury rather than immediately post-injury. For both groups, presuming no advanced directive, definitive airway protection with tracheal intubation should be achieved for patients with concern for severe TBI and high-level SCI, even if the airway is patent and breathing appears adequate at initial evaluation. Patients with acute neurotrauma may present to the operating room (OR) immediately after admission or thereafter with ongoing resuscitation and pending completion of secondary surveys. Serial neurological examinations should include pupillometry (neurological pupillary index: NPI), pupil size and reactivity, GCS score, upper/lower extremity motor and sensory function, and lateralizing signs (paresis, plegia, hyperreflexia). Neuromuscular blockade reversal may be required if tracheal intubation has been established pre-transport [14]. Anesthesiologists should review laboratory data and ensure the availability of blood products. Oxygen saturations in the low 90 s may mask hypoxemia in people of color [16], and end-tidal capnography data underestimates partial pressure of carbon dioxide (PaCO₂) during hypotension; arterial blood gas sampling should be performed to confirm these suspicions. Timely and goal-directed anesthesia care for all patients with neurotrauma is critical. Anesthesiology care is provided along the continuum of trauma care and aims to reduce mortality and improve functional outcomes. Postoperative care should include evaluation of anesthesia care complications for systems improvement.

Principles of Acute Moderate and Severe Traumatic Brain Injury Care

Classification and Pathophysiology

TBI is currently classified by the Glasgow Coma Scale (GCS) score as mild (13–15), moderate (9–12), and severe (GCS 3–8). However, GCS alone may not be a good diagnostic [6] or long-term prognosticator tool [17]. A combination of biomarkers, imaging, and clinical conditions may be required to determine TBI severity [6], and patients can deteriorate from mild or moderate TBI [18] requiring escalation of care. The Brain Trauma Foundation guidelines are an effort to support interdisciplinary consensus during acute TBI care [19]. While there is only one level 1 recommendation to avoid corticosteroids, efforts to create “living guidelines” [20] are expected to update recommendations. These guidelines broadly discuss anesthetic agents as part of ICU care, but anesthesia care in the operating room is not addressed.

TBI can be diffuse or focal, include multiple pathologies (epidural or subdural or intracerebral hematomas, subarachnoid hemorrhage, parenchymal contusions, and diffuse axonal injury), and result in various evolving pathophysiological processes [21]. Following initial neuronal injury, secondary brain injury, characterized by increased inflammatory cytokines, excitotoxicity, and cerebral edema, can lead to cellular apoptosis, worsened inflammation, and cellular necrosis [22]. Efforts to mitigate secondary brain injuries are complicated by the need to address extracranial pathologies in both polytrauma and isolated TBI (Table 2).

Table 2.

Potential pathophysiology, organ system involvement, and complications after acute traumatic brain injury and traumatic spinal cord injury

Organ system	Traumatic brain injury	Traumatic spinal cord injury
Neurological/Psychological	Hydrocephalus, depression, anxiety/agitation, sleep disturbance, cognitive deficits	Spinal shock, paraplegia or Tetraplegia, central cord syndrome, Brown-Sequard syndrome, depression, social isolation,
Cardiovascular	Reduced ejection fraction, prolonged corrected QT interval, global longitudinal strain	Neurogenic shock, Impaired cardiac function, recurrent cardiac arrest, refractory shock, autonomic dysreflexia
Respiratory	Increased risk of VAP, ARDS	Respiratory muscle weakness, respiratory deficits/failure, possible tracheostomy or long-term ventilator requirement, airway hyperreactivity
Gastrointestinal	Dysbiosis resulting in worsening neuro-inflammation, stress ulcers	Acute mesenteric ischemia, Cushing’s ulcer, neurogenic bowel dysfunction
Hematologic	Anemia and coagulopathy of TBI	Anemia, higher risk of thromboembolic events
Endocrinological	Cerebral salt wasting, syndrome of inappropriate antidiuretic hormone, stress-induced hyperglycemia, increased cortisol	Immobilization hypercalcemia, lower levels of endocrine hormones
Immunological	Inflammation, leukocytosis, increased cortisol and immune suppression, decreased autophagy	SCI-induced (neurogenic) immune deficiency syndrome, immune depression, autoimmunity, higher risk of infections, pneumonia and UTI
Dermatological	Scalp injury	Pressure ulcers

VAP: ventilator-associated pneumonia; ARDS: adult respiratory distress syndrome; TBI: traumatic brain injury, SCI: spinal cord injury; UTI: urinary tract infection

Systemic and Cerebral Perfusion Pressure

Cerebral perfusion pressure (CPP) = mean arterial pressure (MAP) minus intracranial pressure (ICP) directly affects cerebral blood flow (CBF). Invasive blood pressure monitoring allows better control over CPP [23]. The goal is to prevent systemic and cerebral hypotension. Definitions of hypotension vary and include variable age-related SBP thresholds. In general, avoiding hypotension (SBP < 90–110 mmHg and CPP < 60 mmHg) is paramount to prevent poor outcomes in severe TBI [24]; recent data suggests targeting an SBP of 110 rather than the earlier target of 90 mmHg. Alternatively a MAP of 80 mmHg can be used [25]. Hemodynamic thresholds are lacking in moderate TBI. Excluding hemorrhage, unexplained hypotension should trigger point-of-care ultrasound for systolic dysfunction assessment [26]. Excessive hypertension may be detrimental given that cerebral autoregulation may be impaired, leading to high ICP, cerebral edema, and/or hemorrhage.

Systemic Oxygenation

Both hypoxia (arterial partial pressure of oxygen [PaO₂] < 60 mmHg) and hyperoxia (PaO₂ > 200–250 mmHg) are associated with poor outcomes [27]. Continuous monitoring via pulse oximetry that correlates SpO₂ > 92% with PaO2 may prevent occult hypoxemia [28].

Ventilation Effects

When cerebral metabolism is normal or high, unwanted hyperventilation can lead to cerebral ischemia, whereas hypercapnia may induce cerebral hyperemia, increase ICP, and worsen cerebral edema [29]. Yet, hyperventilation use is common [20, 30]. Hypercapnia is not a standard treatment [31] and PCO₂ should be maintained between 30–35 mmHg [20]. Correlating end-tidal carbon dioxide (CO2) with PaCO2 may be necessary in patients with shock or pulmonary disease.

Intracranial Pressure (ICP)

Normal ICP ranges from 7–15 mmHg. Hemorrhage and brain swelling increase brain volume, causing intracranial hypertension (ICP > 22 mmHg) [20] resulting in adnormal cerebrovascular reactivity and worsening outcomes [32]. ICP monitoring is recommended to reduce mortality in severe TBI, but international data suggests no benefit compared to sound neurocritical care [33], resulting in low utilization [20, 34, 35]. Individualized ICP threshold-based and timely care may be desirable [20, 34, 36, 37]. Without ICP data, CPP may be over and/or underestimated. When used, local practice utilizes invasive parenchymal ICP monitoring with adjunct use of external ventricular drain to treat ICP crisis. ICP crises should be managed irrespective of the presence of ICP monitoring, and treatments have been described for the ICU setting [38]. Anesthesiologists should know how to use and interpret data from devices that measure ICP and drain cerebrospinal fluid during ICP crises [39].

Cerebral Blood Flow and Metabolism

After acute TBI, CBF has a triphasic pattern with early cerebral hypoperfusion (first 24 h), hyperemia (for 1–3 days), and then vasospasm (> three days) [40]. A mismatch between CBF and CMRO₂ is common, and cerebral metabolic rate of oxygen (CMRO₂) is often lower in the first three days after injury [41]. Patients with TBI usually have a higher ratio of CBF to CMRO₂ and a lower ratio of CBF to cerebral blood volume, suggesting abnormal flow-metabolism coupling. Still, heterogeneity exists between and within patients [42] and with TBI evolution. Current BTF guidelines do not address CBF monitoring. Real-time bedside measures that quantify these physiological changes after severe TBI are not regularly available for clinical use.

Cerebral Autoregulation

Cerebral autoregulation reflects the homeostatic mechanism by which CBF is preserved in relation to blood pressure changes and is often abnormal/absent for weeks after TBI [43]. Thus, CBF may depend on CPP/SBP. While transcranial Doppler (TCD) ultrasonography can intermittently assess cerebral autoregulation (dynamic or static), continuous measures derived from ICP monitor waveforms [44, 45] may help evaluate patient status and treatment effects. Bedside continuous measures of cerebral autoregulation may be used clinically at some centers but are primarily in the research realm; translation is needed to individualize and optimize cerebral perfusion [46–49] during TBI evolution in clinical care. CO₂ reactivity may be impaired after TBI [50] and our usual maneuvers that change PaCO2 may result in undesirable CBF effects. However, there are no bedside tools to personalize ventilation treatments in relation to patient CO2 reactivity readily.

Cerebral Oxygenation

Cerebral oxygenation reflects the balance between oxygen supply (CPP, CBF) and demand (CMRO₂ and high ICP). Cerebral oxygenation can be measured by brain tissue oxygenation monitors (PbtO₂; < 10 mmHg reflects cerebral ischemia) [51], near-infrared spectroscopy (NIRS) for trends, and jugular venous saturation monitors (SjVO₂ < 50 mmHg reflects ischemia) [14, 52–54]). PbtO₂ response patterns vary in response to MAP augmentation [55], the role of PbO₂ and use of FiO₂ in increasing PbtO₂ is unclear, and the BOOST 3 Trial studying bundled approach to increasing PbtO₂ is underway [54, 56]. Without coagulopathy, ICP monitoring should be considered in patients with acute moderate-severe TBI undergoing extracranial procedures to guide CPP management. When used, PbtO₂ monitors offer an opportunity for physiological manipulation to prevent cerebral hypoxia.

Electrolytes, Hyperosmolar Therapy, and Metabolic Effects

Electrolyte imbalances can cause complications, particularly with the administration of hyperosmolar therapy (mannitol or hypertonic saline) for intracranial hypertension. Hypernatremia is common after hyperosmolar therapy and sodium levels of > 155 mEq/L, but some studies suggest hyperchloremia (> 125 mEq/L) should be avoided [57]. Early mannitol use is associated with acute kidney injury [58]. Some studies have shown better CPP profiles and a more significant reduction of ICP [59, 60] with hypertonic saline compared to mannitol. Still, metanalyses show that hypertonic saline may be equivalent to mannitol for other clinical outcomes except for the observed hypernatremia and hyperchloremia [57]. Intraoperative hyperglycemia is common [61] and anesthesiologists should aim to maintain euglycemia, avoiding extremes of glucose. Thresholds of glucose < 70 mg/dL and over 180 mg/dL likely need treatment.

Temperature

Fever increases CMRO_2, and normothermia is the general goal. Hypothermia is associated with arrhythmias and coagulopathy but may be used to reduce refractory high ICP. Rapid rewarming of hypothermia causes arrhythmias and acidosis. There is no benefit of early, prolonged hypothermia [62, 63] and hypothermia (≤ 35⁰C) on admission may be associated with significantly higher mortality in patients with TBI [64]. Prophylactic hypothermia is not recommended.

Preoperative Assessment

Beyond ATLS recommendations, anesthesiologists should ensure operating room readiness, perform a thorough preoperative assessment, and develop an intraoperative care plan that anticipates the physiological consequences of TBI. Cardiovascular compromise and hemorrhagic shock from extracranial injuries may compromise cerebral perfusion [20] and challenge tracheal intubation and anesthesia care. Anesthesiologists may assume care in the emergency departments, intensive care units, or operating rooms to least delay in care [20, 65–68]. Anesthesiologists should obtain a TBI-specific history of present illness, comorbidities, clinical course, and treatments after TBI to determine the need for intraoperative care. Specific attention to signs and symptoms of elevated ICP should be noted and addressed and intraoperative positioning where patients may be supine or prone.

Intraoperative Anesthesia Care

Induction of Anesthesia and Tracheal Intubation

Patients with TBI receive general anesthesia for emergent craniotomy, decompressive craniectomy, and/or extracranial surgeries. In emergent tracheal intubation, rapid sequence intubation (RSI) may prevent aspiration risk in emergent tracheal intubation. However, modified RSI (low tidal volume and airway pressure breaths ± cricoid pressure) may be used if ICP is high. Systemic and cerebral hypotension should be avoided/expediently corrected using intravascular fluids and/or vasoactive agents. Video laryngoscopy may facilitate faster tracheal intubation, and difficult airway equipment should be readily available.

Sedation or anesthetic induction with incremental doses of etomidate, low-dose propofol, and/or ketamine is common and safe [69, 70]. Fentanyl may be used during induction to blunt hypertensive responses to laryngoscopy [71]. Long-acting opioids should be avoided at the end of the case if a postoperative examination of neurological status is needed. Potential high ICP risks of succinylcholine may be mitigated by transient hyperventilation and used if difficult airways are suspected [69]. Nasotracheal intubation should not be used when skull fracture status is unknown/suspected. Anesthesiologists can loosen the anterior portion of the cervical immobilization device and maintain in-line cervical spine stabilization to facilitate tracheal intubation.

Oxygenation and ventilation strategies must prevent and correct hypoxia. Low tidal volume ventilation with positive end-expiratory pressure improves oxygenation, respiratory mechanics and decreases post operative pulmonary complications [72]. Recruitment maneuvers and positive end-expiratory pressure may increase high ICP [73] which should be used cautiously. Hypocapnia (PaCO₂ < 30 mmHg) can be used as a bridge to definitive treatment [20] of high ICP. Hourly arterial blood gas evaluation is recommended to detect hypocarbia or hypercarbia; arterial-end tidal CO₂ gradients increase during hypotension.

Maintenance of General Anesthesia

There are no large studies comparing intravenous vs. < 1 minimum alveolar concentration (MAC) volatile anesthesia for maintenance of general anesthesia in TBI. Nitrous oxide is not recommended due to increased CBF, increased CMRO₂, and potentially increased ICP. Total intravenous anesthesia (TIVA) with propofol may cause cerebral vasoconstriction and worsen cerebral ischemia in refractory ICP, making low-dose volatile agents preferable or adjuncts. Ketamine may prevent the progression of neuronal injury [74], dexmedetomidine and propofol may be equally effective for ICP and CPP control [75], and dexmedetomidine anesthesia may decrease brain injury markers [76, 77]. Use of propofol with remifentanil may have a role in neuroprotection in severe TBI [78] and propofol may reduce the risk of swelling in elective craniotomies [79], but sevoflurane use may result in less hypotension and decreased inflammation than propofol [80]. Typically, general anesthesia can be maintained utilizing a combination of < 1 MAC of volatile anesthetics (VA) to minimize cerebral vasodilation, short-acting opioids, and neuromuscular blockade (NMB), unless ICP is refractory, when TIVA may be used.

Intravenous Access and General Monitoring

Intravenous access (two large-bore peripheral intravenous catheters) should be obtained early in TBI anesthesia care. Some patients will require central venous access at the start of and/or end of the case, but line placement should not delay decompression. Monitoring should include electrocardiogram, pulse oximetry, end-tidal carbon dioxide, blood pressure (preferably invasive), neuromuscular blockade, and core temperature. Neither jugular venous oximetry nor brain tissue oxygenation is standard practice in TBI anesthesia care. Still, it may provide helpful patient-centered information to clinicians, and brain tissue oxygenation technologies show promise.

Hemodynamic Goals

Intraoperative hypotension is not desired but is common [81, 82]. Neurogenic shock, cardiac dysfunction, and or have been prescribed beta-blockers, which may reduce mortality and improve outcomes [83]. Hemodynamic goals in TBI care are primarily extrapolated from BTF guidelines [20]. In patients with extracranial injuries complicated by moderate-severe TBI and/or comorbidities, hemodynamic goals may conflict [14]. Decompression may cause significant hypotension, leading to asystole, but it can be prevented with pre-decompression administration of intravenous fluid (or blood if needed) administration before durotomy. ICP monitors may be placed at the end of surgery (after confirmation of normal coagulation) or may present for anesthesia care with an indwelling ICP monitor. ICP monitoring allows for CPP determination [84].

Vasopressors and Intravenous Fluids

There are no vasopressor recommendations [20, 85–87] specific to TBI care, and the vasoactive agent of choice may depend on cardiac function. Vasopressin may result in less hyperosmolar therapy needed, but this remains controversial [85, 88]. Although there are no recommendations for intravenous fluids, isotonic fluids are preferred. Albumin is associated with higher mortality and should be avoided [67, 89].

Intracranial Hypertension

High ICP, defined as ICP ≥ 22 mmHg, may manifest with respiratory changes, pupillary changes, hypertension, and bradycardia, but arrhythmias and asystole may also occur. ICP crises should be recognized and managed promptly because of the risk of cerebral herniation and death [90].

Hyperosmolar Therapy

Mannitol or hypertonic saline (2% and 3%, or 23.4% [91]) may be used [92, 93]. Serial monitoring of sodium levels is required during the administration of hyperosmolar therapy. Mannitol use may result in hyponatremia and hypovolemia, necessitating isotonic fluid resuscitation, and is contraindicated in patients with renal failure. Treatment may be administered through peripheral or central venous lines.

Transfusion

Preoperative plasma administration may improve outcomes in blunt severe TBI through immune modulation and reduced endotheliopathy [94]. Anemia is associated with worse outcomes, but there are no standard transfusion thresholds [95] in TBI. The range of Hgb 7–9 g/dL is acceptable [96] and a trial of liberal vs. restrictive strategy is underway [97]. Thromboelastography or ROTEM may detect coagulopathy, but standard hemorrhage panel use is acceptable if turnaround times are rapid [98–100]. While uncommon, given the use of balanced blood transfusion, Factor VII and tranexamic acid may both be safely used to correct coagulopathy [68, 101, 102].

Post Procedure and Postoperative Care

Patients with acute moderate-severe TBI often remain sedated and endotracheally intubated at the end of surgery for continued airway protection and ventilation management since the TBI condition evolves (i.e., Cerebral edema). For endotracheally intubated patients, sedation improves tracheal tube tolerance and prevents increased ICP during transport to radiology or the intensive care unit. Residual neuromuscular blockade may confound the neurological examination, and anesthesiologists may reverse the neuromuscular blockade on a case-by-case basis. The use of post-procedural intraoperative CT scans prevents off-site transport-related second injuries and may also result in patients returning to the operating room based on findings. TBI can result in chronic pain states, and the use of collaborative care models may be helpful [103] to patients.

Acute Traumatic Spinal Cord Injury

Epidemiology

The incidence of SCI in the US is approximately 54 cases/million/year [104]. Motor vehicle crashes, falls, and violence account for 85% of SCI cases. Cervical SCI is most common, occurring in more than half [105] of SCI patients. SCI occurs disproportionately high in non-Hispanic Blacks, highlighting the health disparity and urgent need for primary prevention.

Anatomy, Physiology & Pathophysiology

Like TBI, Primary SCI results from mechanical forces, causing compression, distraction, and/or cord disruption, followed by secondary injury triggered by systemic and local factors such as hypoxia or hyperthermia. This cascade leads to neuroinflammation, excitotoxic damage, and cell death expansion. Targeting secondary injury is crucial for therapeutic interventions to minimize damage and promote recovery.

Physiological changes in SCI vary based on the level and completeness of injury. Higher SCIs, particularly from mid-thoracic levels, are associated with increased cardiovascular and respiratory disturbances. Table 2 details the pathophysiology and organ systems involvement in SCI.

Timely airway management prevents life-threatening conditions and limits SCI. Indications for tracheal intubation include respiratory failure from high thoracic or cervical SCI or concomitant injuries such as chest injuries or TBI. Despite evidence suggesting that all airway maneuvers, including jaw thrust and bag-mask ventilation, cause movement of the cervical spine, proof that these motions translate to exacerbation of neurologic injury is lacking [106]. In emergency settings, rapid sequence induction with manual in-line stabilization (MILS) is regarded as the standard of care [107, 108] under the precautionary principle of preventing further injury. Studies suggest video laryngoscope (VL) [109] and flexible scope intubation [110] reduce cervical spine movement compared to direct laryngoscope (DL), but no technique has shown clear superiority in preventing further neurologic injury [111]. VL is recommended for higher first-pass success, especially with MILS [112]. Data from 252 patients with unstable cervical SCIs support VL as the most used technique, with no identified neurological injuries attributable to airway management [113].

Breathing can be variably impaired by the spinal cord and muscles of respiration denervation with severity depending on injury level and completeness. Complete injury above C3 can lead to apneic respiratory arrest due to phrenic nerve (C3–5) involvement, while lower segment injuries cause hypercarbic respiratory insufficiency. Injuries below T12 usually do not affect breathing. Respiratory complications may worsen days post-injury due to factors like ascending level involvement [114], neurogenic pulmonary edema, bronchospasm, increased secretion, and decreased mucus clearance [115], highlighting the importance of ongoing monitoring and treatment. Prompt tracheal intubation and mechanical ventilation are required for patients with complete SCI above C3. Most patients with injury at C3-C5 need initial tracheal intubation, but this may not be required in patients not in respiratory distress. Instead, close monitoring and aggressive respiratory therapy are recommended [116].

Circulatory disturbance in trauma encompasses hemorrhagic or cardiogenic shock, with neurogenic shock additionally occurring in SCI, particularly above the T6 level [117]. Reduced sympathetic output (T1-L2), particularly the cardiac accelerator fibers emerging from T1 to T4 spinal segments, and increased parasympathetic activity led to bradycardia and vascular dilation, exacerbating spinal cord hypoperfusion. Prompt hemodynamic resuscitation involves intravenous fluid boluses to optimize preload and vasopressor titration to support blood pressure, ideally under close monitoring. Norepinephrine is favored over dopamine for its cardiac safety [118], and it is favored over phenylephrine for spinal cord perfusion and maintenance of heart rate benefits [119]. Current guidelines recommend maintaining a MAP of 85–90 mmHg for seven days post-SCI [120, 121]. However, this is supported mainly by case series and observational studies. Theoretical basis suggests increasing blood pressure may improve spinal cord blood flow and reduce ischemic injury, the benefit of vasopressor use alone is unclear. The ongoing RCT (TEMPLE study) [122] aims to clarify optimal blood pressure targets for SCI outcomes, with results expected in 2024.

Disability and neurologic deficits (motor, sensory, and autonomic) should be thoroughly evaluated and documented before administering anesthesia, provided the patient’s physiological stability allows. Structured examination of the spine and spinal cord usually occurs during secondary surveys. It should follow the International Standards for Neurological Classification of Spinal Cord Injury (ISNCSCI) published by the American Spinal Injury Association (ASIA). The sensory level is determined by testing touch and pinprick according to dermatomal distribution, while the motor level is assessed for both levels, correlating key muscle motion to spinal root [123]; and the motor strengths. Neurological level is then determined based on bilateral intact of both motor and sensory function, and ASIA impairment scale assigned based on completeness of injury, from A complete, to B sensory incomplete, C&D motor incomplete of different strength levels. Careful positioning is essential before definitive treatment and during transport, prioritizing spine alignment maintenance and concurrently aiming to prevent pressure injuries [124].

Steroid administration in SCI remains controversial. Systematic reviews indicate limited to no benefit of methylprednisolone, with significant increases in adverse events such as gastrointestinal bleeding and respiratory tract infection [125]. Most guidelines [121], including those from the American Association of Neurological Surgeons (AANS) [120], advise against methylprednisolone use. At the same time, AOspine suggests 24 h of methylprednisolone (30 mg/kg bolus and 5.4 mg/kg/hr. infusion for 23 h) as a treatment option if initiated within 8 h of injury [126].

Early surgical decompression, within 24 h of injury, seems to be associated with neurological recovery in SCI [127], including central cord syndrome [128], and is currently recommended [121, 129]. However, benefits should be weighed against optimizing concurring injuries and medical comorbidities.

Perioperative Care of the Patient with Spinal Cord Injury

Key anesthetic goals for spine decompression aim to prevent secondary injury (from hypotension, hypoxia, and hyperglycemia), optimize surgical conditions and intraoperative neuromonitoring (IONM), and maintain homeostasis. Anesthesia should be tailored based on SCI level and medical conditions. Arterial cannulation and central venous access may be necessary for monitoring and vasopressor infusion. While halogenated volatile anesthetics up to 0.5 MAC can be used with IONM in patients without preexisting neurologic impairment, they may abolish sensory or motor-evoked potentials in those with baseline deficits. Total Intravenous Anesthesia (TIVA) with increment dosage adjustment is typically preferred [130].

The surgical position varies according to spinal level and approach. Common positioning goals are preventing associated injuries, particularly of the eyes, peripheral nerves, and tongue, especially under neuromonitoring, and avoiding increased venous pressure and associated bleeding at the surgical site.

Intravascular volume assessment can be challenging in prone positions. Goal-directed therapy using dynamic parameters like pulse pressure variation (PPV) is recommended to optimize fluid status. PPV > 15% predicts volume responsiveness in prone positions. Strategies to minimize blood loss and transfusion while maintaining oxygenation should be pursued. Prophylactic tranexamic acid showed an association with decreased blood loss [131] and is recommended for complex procedures [130], with dosing ranging from 5–15 mg/kg bolus and 1–2 mg/kg/h infusion [130, 131].

Multiple factors, such as SCI level, concomitant injury, and surgery extent, influence extubation timing in SCI patients. Respiratory complications, particularly in cervical SCI, are prevalent. Aggressive therapy and close monitoring can enhance outcomes. Early tracheostomy (within seven days) seems beneficial for patients with high cervical SCI by reducing mechanical ventilation and length of stay [132]. Blunt cerebrovascular injury (BCVI) often accompanies blunt cervical trauma and is a risk factor for increased mortality and ischemic stroke [133]. Treatment aims to prevent neurological ischemia, including early antithrombotic therapy initiation [134] and selective endovascular/surgical interventions. Chronic pain occurs in more than half of SCI patients and can significantly impact their quality of life. Therapy should start ideally pre-operatively and incorporate both physical therapy and a multimodal pharmacologic approach.

What’s New?

Patients with SCI are at higher risk of refractory neurogenic shock, especially with high cervical spinal cord injury, due to cardiovascular autoregulatory disturbance [135]. Resuscitative endovascular balloon occlusion of the aorta (REBOA) is a well-known intervention for non-compressible torso hemorrhage refractory to blood product resuscitation. Recently, it has been used as an adjunct to prevent prolonged hypotension and the risk of further anoxic spinal cord injury in neurotrauma patients. In 2018, Gray et al. reported the first successful use of Zone 1-REBOA (from the origin of the left subclavian artery to the celiac artery) in a patient with neurogenic shock due to C5 comminuted fracture with cord contusion [136]. Kim et al. reported 3 cases of Zone 1-REBOA use in neurotrauma patients with significant improvement in blood pressure [137]. However, the long duration of Zone 1-REBOA may result in spinal cord ischemia in animals [138]. Parra et al. recommended using Zone 3 (from the lowest renal artery to the aortic bifurcation) REBOA. They limited to 30 min in refractory cases of traumatic neurogenic shock to aid in the resuscitation and minimize the risk of spinal cord ischemia [139]. Recently, the leadless pacemaker has been placed in SCI patients with recurrent cardiac arrest [140]. A systematic review and meta-analysis showed that using the leadless pacemaker (Micra) is associated with a low risk of complications and good electrical performance up to 1-year post-implantation [141].

Spinal Cord Hemodynamic Monitoring

Traumatic SCI management aims to prevent ischemic secondary injury and improve neurologic outcomes by maintaining MAP at 85–90 mmHg because MAP level positively correlates with neurologic recovery improvement [142]. However, higher MAP alone does not effectively improve spinal cord perfusion; the spinal cord perfusion pressure (SCPP) target of 60–65 mmHg strongly predicts neurological recovery after SCI [143]. SCPP is consistently higher in SCI patients with a CSF drainage group than with no CSF drainage group [144]. In 2020, the TRACK-SCI study reported the first SCPP implementation as a clinical standard of care in acute tSCI patients [145]. The spinal pressure reactivity index (sPRx) is a surrogate index of spinal autoregulation. It can be used to determine the optimal MAP (when sPRx is < 0.3) in patients with tSCI [146]. The SCPP measurement requires obtaining the intrathecal pressure, and the placement of an invasive intrathecal catheter has its complications [147]: epidural hemorrhage, hematoma formation, [148] spinal cord compression, even further damage to the injured spinal cord, which may limit the application of SCPP.

Near-infrared spectroscopy (NIRS) has been used in cardiac and non-cardiac surgeries to evaluate cerebral oxygenation. Amiri et al. were the first to use intraoperative NIRS with indocyanine green tracer technique to identify an increase in the spinal cord pressure in response to hypercapnia [149]. Recently, Shadgan et al. used the non-invasive transdural NIRS sensor to monitor oxygenation of the injured cord in a pig model and found a significant correlation between NIRS-derived oxygenation and tissue oxygenation percentage of invasive intraparenchymal sensors [150], which shows the potential utility of NIRS in acute traumatic SCI patients.

Timing of Surgery

The timing of decompressive surgery in SCI is controversial

Recently, several studies recommended “ultra-early” surgery (< 8–12 h) based on significant improvement in AIS grade postoperatively [151–153] and higher SCIM scores in bladder and mobility function [148]. However, these are single-center studies with small sample sizes. The SCI-POEM study, the largest prospective, multicenter observational cohort study, initiated in 2011, found that early surgical decompression (< 12 h) was not associated with neurological improvement at 12 months from tSCI patients [154]. The 2023 AO Spine-Praxis Guidelines in Acute Spinal Cord Injury recommended early decompressive surgery (24 h) for adult patients with acute SCI regardless of level with moderate quality of evidence, and recommended against ultra-early surgery based on small sample sizes and inconsistency of the evidence [155].

Emerging Concepts

Data science and Artificial Intelligence, serum metabolome & biomarkers [156], translational models, classification systems, brain organ crosstalk, and non-invasive ICP monitoring techniques, neuromonitoring represent emerging areas of research, education, and practice (Table 3). Results of the multicenter international IMPRESSIT (Invasive vs. Non-Invasive Measurement of Intracranial Pressure in Brain Injury) Trial [NCT02322970] are pending [157].

Table 3.

Emerging areas for research, education, and practice in acute traumatic brain injury and acute traumatic spinal cord injury

Acute traumatic brain injury	Acute traumatic spinal cord injury
Invasive and non-invasive CPP, ICP, and brain tissue oxygenation monitors [85]	New therapies: ischemia prevention (hyperbaric oxygen [173], nerve regeneration (stem cell therapy [174]), immunomodulation/therapy [175]), minimizing inflammation, controlling cytotoxicity, data science and machine learning [176], diagnostic RNA techniques [177]
Artificial intelligence/machine learning in improving predictions of decline/secondary injury [158, 159]	Combinatorial approaches to target diverse aspects of SCI pathology
Gut neurotransmitter effects	Robotic exoskeleton devices for rehabilitation and mobility Continued multifactorial mechanisms, including molecular, cellular, inflammatory
Blood pressure management,	Acute phase: multidisciplinary cooperation
Alternative substrates for brain metabolism [160]	Long-term: structured educational program during rehabilitation
Serum metabolome and biomarkers (UCH-L1, GFAP, neurofilament light) [156, 161]	Percutaneous electrical stimulation of spinal cord, epidural electrical stimulation to facilitate sensorimotor network functionality, early gabapentin in tSCI to promote neurological recovery, early local hypothermia,
Red blood cell defect monitoring as a form of ‘biomarker’ of TBI [162]	Rural vs urban areas, access to care, gender, racial and ethnic minority, insurance types
Catecholamine versus inflammatory effects	Role of spinal cord hemodynamic and perfusion monitoring, Regenerative medicine with human induced pluripotent stem cells therapy for acute/subacute SCI. Robotic exoskeleton rehabilitation and mobility devices
Organ crosstalk (brain–heart/brain-gut)
Best animal model
Classification schemes for diagnosis and prognosis [5]
Brain function monitoring [163]
Cerebral oximetry indices [164]
Frailty measures
Imaging modalities in diagnosis, care, and prognostication
Organizational factors, process flows
Barriers and facilitators to care
Implementing evidence-based guidelines
Variation in acute care
Prevention of chronic conditions
Age effects (older adults)
Gender and intersectionality
Socioeconomic status
Equitable access to acute and post-injury care
Environmental causes and consequences
Translational models [165] and mesenchymal stromal cells [166]
Multifunctional resuscitation cocktails including hydroxyethyl starch solutions in animal models [167]
Selective brain cooling [168]
Alternative volatile anesthetic use (Xenon) [169]
Cerebral autoregulation monitoring [48]
Alternative medical treatments for cerebral edema [170]
Endothelial cell protective effects of dexmedetomidine [171]
Hypertonic sodium pyruvate resuscitation [172]

Conclusions

Timely and goal-directed care is critical for all patients requiring urgent/emergent anesthesia care. Anesthesia care for acute neurological injury should incorporate understanding the evolution of traumatic brain injury and spinal cord injury that translates to preoperative preparation, hemodynamic resuscitation, prevention of second insults, and safe transport between care settings. Anesthesia care should support optimizing patient outcomes. Best practices involve extrapolating data from the intensive care unit setting since there is a lack of research addressing anesthesia care for acute neurological injury. There are opportunities to generate data to support evidence-based anesthetic care.

Data Availability

No datasets were generated or analysed during the current study.