The severity of primary injury from neurotrauma is the major factor that determines the final neurological outcome. Secondary neurological injury caused by physiological effects that develop after the initial primary injury, contributes to the worsening of neurological outcome. Minimizing secondary neurological injury is the goal of the Anesthesiologist. Post injury hypotension , hypoxemia, hyercarbia, hypocarbia, hyperglycemia, hypoglycemia, and coagulopathy can all develop after neurological injury and contribute to final neurological outcome.

Traumatic brain injury is a contributing factor in 30.5 % of all injury related deaths in the United States, it occurs more often in young children, aged 0–4 years, adolescents aged 15–19 years, and elderly aged over age 65 [1–3]. Evidence based guidelines for both prehospital and perioperative management of patients with traumatic brain injury are published and updated. [4] Unfortunately, in spite of significant improvements in treatment of head injury in both the prehospital and hospital environment, the prognosis of patients with severe head injury still remains poor making prevention of head injury a high priority.

Primary traumatic neurological injury is the damage caused by the initial trauma from mechanical impact to the skull and brain tissue due to acceleration, deceleration, rotation, or penetration. This injury results in brain contusion, skull fracture, expanding intracranial hematoma, or diffuse axonal injury. The primary injury then initiates inflammatory processes with edema and excitotoxicity which result in further increases in intracranial pressure and decreased cerebral perfusion. [6–8] Secondary injury progresses after initial injury resulting in additional brain damage and worsened neurological outcome. The IMPACT study meta-analysis demonstrated that hypotension (Systolic pressure <90 mm Hg) and hypoxia (PaO₂ < 60 mm Hg) were associated with a worse prognosis. [8–10] The duration of intraoperative hypotension along with hypocapnea, hypercapnea, hyperglycemia, and hypoglycemia can all worsen secondary brain injury [8, 11–15] Coagulopathy is commonly associated with neurotrauma. Patients with severe combat-related trauma and isolated traumatic brain injury had worse coagulopathy than non-traumatic brain injury trauma [16]. Patients with traumatic brain injury with coagulopathy had worse outcomes than those with traumatic brain injury without coagulopathy [17–20]. Since secondary head injury is treatable, perioperative management with rapid evaluation, continuation of resuscitation, early neurosurgical intervention, intensive monitoring, and anesthetic planning all play a role in the treatment of neurotrauma.

A resuscitation continuum begins at the point of injury, continues on to the operating room then to the intensive care unit. Specialized care in designated trauma centers has been demonstrated to improve outcome in patients with serious injury (Injury Severity Score > 15, Glasgow Coma Scale Score < 9) [21]. Patients taken directly to a trauma center have a lower mortality than those taken to another treatment facility first and then transferred to a level one trauma center [22] Stabilization and emergency transport requires trained emergency responders that have the skills necessary to treat hypoxia and hypotension. Proficiency in airway and both blood pressure and volume management are required in first responders. Targeted prehospital ventilation is associated with lower mortality after severe TBI [23]. Forward critical care resuscitation is an important component of trauma care in the military. The use of physician based emergency evacuation teams in the British military has resulted in improved survival in traumatic brain injury thought attributable to early expert emergency physician anesthesia and ventilation [24]. “Damage control” emergency trauma treatment takes it name from the US Navy term for emergency control of only systems required to prevent a damaged ship from sinking. This consists of rapid abbreviated surgery followed by resuscitation and aggressive correction of the “lethal triad” of coagulopathy , hypothermia, and acidosis. Damage control neurosurgery consists of stopping intracranial bleeding, evacuation of intracranial hematoma, early surgical debridement to limit wound contamination and possible decompressive craniotomy and surgical reduction of increased intracranial pressure [25].

Initial assessment and treatment in the emergency department needs to include evaluation of the airway with confirmation of proper placement of an endotracheal tube placed by the transport team [23]. The ability to ventilate along with assessment of both volume status and blood pressure is followed by a rapid assessment of neurological status. Mental status, Glasgow Coma Scale score and pupillary responses should be assessed. Evaluations for both cardiac and noncardiac causes of hypotension need to be considered especially frank bleeding, pneumothorax and pericardial tamponade. Consent, allergies, last meal, preexisting medical history, medications and laboratory assessment should be obtained as time permits. Resuscitation should continue on the way to the operating room.

Patients with traumatic brain injury will most often need endotracheal intubation. All traumatic brain injury patients should be considered to have a full stomach and possible cervical spine injury. A lower the Glasgow Coma Scale Score and a greater extent of facial fractures are associated with an increased chance of cervical spine injury. This is especially true with a GCS score less than 8 on presentation [26, 27]. The technique for tracheal intubation is determined by the urgency of the case, the expertise of the Anesthesiologist and the available airway resources. A rapid sequence intubation, with in line cervical stabilization, with the use of cricoid pressure in the most common technique. Use of video assisted laryngoscopy is becoming more commonplace and can provide a helpful alternative to direct laryngoscopy. Nasal intubation is usually avoided in patients with a coagulopathy , nasal or skull fractures. The ability to create a surgical airway should always be available.

Instrumentation of the airway is often greatly facilitated by the use of anesthesia induction agents and muscle relaxants. Selection of the best induction agent is based on level of consciousness, need for a muscle relaxant and hemodynamic stability. All of the induction drugs can be associated with significant hypotension and should be avoided in patients with significant hemodynamic stability. Midazolam and scopolamine, which are commonly used in trauma patients with significant hemodynamic instability, are often avoided in significant head injury due to their longevity and the lack of reversal agents. Flumazenil is often relatively contraindicated in head injury due to its ability to facilitate seizures [28].

Propofol is by far the most common drug used for anesthesia induction prior to intubation [29]. Etomidate and where available sodium thiopental can also be used. All of these agents decrease the systemic response to intubation, decrease cerebral metabolic rate for oxygen, and blunt the increase in intracranial pressure that can be seen with laryngoscopy. Etomidate does provide improved hemodynamic stability when compared to propofol or sodium thiopental, however, its use is associated with adrenal insufficiency [30, 31]. Ketamine is associated with better hemodynamic stability but it is uncommonly used in neurosurgical trauma due to its longer half life, its association with increased cerebral blood flow, increased intracranial pressure and focal increases in cerebral metabolic rate. Outcome data contraindicating the use of ketamine in the neurosurgical patient has been questioned [32]. Neuromuscular blockade is commonly performed for laryngoscopy with either the depolarizing neuromuscular blocker succinylcholine or the non depolarizing neuromuscular blockers rocuronium or vercuronium [33]. Succinylcholine administration has been associated with an increase in intracranial pressure, however, the clinical significance seems to be marginal at best. The significance of hypoxia and hypercarbia from hypoventilation are more likely to result in worse clinical outcome then a small transient rise in intracranial pressure [34].

Intraoperative anesthetic management consists of the management of physiological parameters as established by the Brain Trauma Foundation and the Multidisciplinary Task Force for Advanced Bleeding following severe injury with appropriate anesthetic agents [35]. Hypotension should be avoided and a systolic blood pressure of greater than 90 mm Hg should be maintained. Hypoxia should be avoided. The PaO₂ should be kept greater than 60 mm Hg and the oxygen saturation should be kept greater than 90 %. Hyperventilation should be avoided unless being used to acutely decrease intracranial pressure . Mannitol should be used when acute treatment of increased intracranial pressure especially when signs of transtentorial herniation or progressive neurological deterioration are not attributable to extracranial causes. Hypertonic saline should be considered as a treatment modality in patients with increased intracranial pressure. Prophylactic hypothermia is not associated with decreased mortality. Moderate hypothermia (33–34 C) beginning within 8 h of traumatic brain injury for between 24 and 48 h could be considered as a treatment for refractory increased ICP with rewarming slower than 5 C per hour [35]. Hyperglycemia after traumatic brain injury is associated with worse outcomes. A target glucose range of between 80–180 mg/dl is reasonable [36–38].

Hyperthermia should be avoided. Intracranial pressure should be monitored in patients with severe traumatic brain injury and an abnormal CT scan or in patients with a normal CT scan if two of the following are present: Age greater than 40 years, motor posturing, or systolic pressure less than 90 mm Hg [4]. Cerebral spinal fluid drainage through and external ventricular drain can be used for refractory increased intracranial pressure if the basal cisterns are open, and there is minimal evidence of mass lesion or shift on imaging studies. If intracranial monitoring is in place, cerebral perfusion pressure should be maintained between 50 and 70 mm Hg. Increase in oxygen delivery should be performed if possible when brain tissue oxygen tension is less than 15 mm Hg or jugular venous saturation is less than 50 %. In patients with severe traumatic brain injury, high dose methylprednisolone is associated with increased mortality and contraindicated [39].

The anesthetic is performed with the knowledge of the pharmacodynamics and pharmacokinetics of the intravenous and volatile anesthetics used. Volatile agents (isoflurane, sevoflurane, desflurane) decrease cerebral metabolic rate while increasing cerebral blood flow. They uncouple autoregulation. However, at less than one MAC these affects are minimal and all three agents can be used at low doses in patients with traumatic brain injury [40]. IV anesthetic agents including propofol , etomidate , and thiopental decrease cerebral blood flow, cause cerebral vasoconstriction and decrease cerebral metabolic rate. All can be used in head injury. The FDA recommends against the use of a propofol infusion for the management of refractory intracranial hypertension due to the possibility of propofol infusion syndrome [41]. Etomidate is associated with a reduction in ICP and significant improvements in cerebral perfusion pressure with reductions in mean arterial pressure. Adrenal suppression is associated with the use of etomidate [42]. Ketamine , unlike the other IV anesthetic agents, has a longer half life, increases cerebral blood flow and cerebral metabolic rate. In spite of this, it is being used in some centers for head injury due to its ability to maintain blood pressure [32, 43]. Nitrous oxide can increase cerebral metabolic rate and cause cerebral vasodilation with increased ICP. Transient myelopathy has been described in patients with B12 deficiency nitrous oxide. Data is lacking showing its use causes worsening outcome and institutions with a long history of administering nitrous oxide continue with its use [44–46]. Opioids provide excellent hemodynamic stability. Although many in vitro and animal models have demonstrated cerebral protection from anesthetic agents secondary to cerebral ischemia, clinical data to suggest any particular anesthetic agent provides improved clinical outcome in patients with head injury is lacking [47, 48].

Anesthetic management will include arterial catheterization for careful blood pressure monitoring as well as blood gas and chemistry analysis during surgery. Central venous access is indicated when required for resuscitation or for vasopressor administration. Timely placement of invasive monitors is important. Placement of access should not significantly delay emergent intracranial procedures. Monitors of cerebral oxygenation can be helpful especially if significant hemodynamic instability is expected or if hyperventilation is used to control intracranial pressure . Jugular venous oximetry, brain tissue oxygenation, and cerebral oximetry can be used for this purpose [49–53].

Hypotension should be avoided and the systolic blood pressure should be maintained at greater than 90 mm Hg while maintaining a cerebral perfusion pressure between 50 and 70 mm Hg. A mean arterial pressure of greater than or equal to 80 mm Hg should be targeted in patients with combined hemorrhagic shock and severe head injury. (GCS < 8) [35]. Hypotension occurring during the first 6 h after head injury has the highest prediction of poor neurological outcome at discharge [54]. Euvolemia, maintained with non glucose containing isotonic crystalloid solutions, should be maintained. Albumin has not shown to be preferred over crystalloid solutions [55]. 3 % hypertonic saline should be considered as a treatment modality in patients with significant increases in intracranial pressure either by bolus or continuous infusion, however it has not been associated with improved outcome over normal saline [35]. Hypertonic saline may be a more effective treatment for increased intracranial pressure management than mannitol [56]. Mannitol should be used only as a short-term acute therapy for increased intracranial pressure . Vasopressors are used to maintain mean arterial pressure and should be used early if blood pressure does not respond to volume treatment [35]. Phenylephrine, norepinephrine, dopamine, and occasionally vasopressin are used and are often institution specific. Current evidence does not support the use of one vasopressor over the others [57, 58]. Hypothermia at 33–35 °C with duration of greater than 48 h with rewarming lasting 24 h and cerebral perfusion pressure greater than 50 mm Hg may improve outcome. This is especially true for head injury patients with a Glasgow Coma Scale of between 4 and 7 [59–62].