Anesthesia for patients with acute traumatic brain injury

INTRODUCTION — Patients with severe traumatic brain injury (TBI) frequently have other traumatic injuries to internal organs, lungs, limbs, or the spinal cord. Thus, the management of the patient with severe TBI is often complex and requires a multidisciplinary approach.

Anesthesiologists are involved in the care of patients with TBI in various situations, including but not limited to resuscitation and stabilization in the emergency department (ED), sedation and anesthesia for diagnostic imaging, craniotomy or decompressive craniectomy, extracranial surgery, and intensive care management.

Surgery and anesthesia may subject the injured brain to new, secondary insults such as hypotension, hypoxemia, hypo- or hypercarbia, fever, hypo- or hyperglycemia, and/or increased intracranial pressure (ICP) that may adversely impact outcome.

This topic will discuss the intraoperative anesthetic management of patients with acute TBI. Epidemiology and pathophysiology, prehospital management, general concerns for anesthesia for craniotomy, and anesthesia for acute spinal cord injury are discussed separately. (See "Management of acute moderate and severe traumatic brain injury" and "Anesthesia for craniotomy in adults" and "Traumatic brain injury: Epidemiology, classification, and pathophysiology" and "Anesthesia for adults with acute spinal cord injury" and "Anesthesia for adult trauma patients".)

PREOPERATIVE EVALUATION — Preoperative evaluation for patients with TBI should include an evaluation of the type and severity of TBI, identification of other associated injuries, review of relevant imaging and laboratory findings, and the identification of any secondary insults. Patients with TBI may require surgery for other associated injuries (eg, orthopedic, abdominal, or thoracic). Even if such procedures are delayed beyond the immediate postinjury period, the goals for anesthesia should include prevention of secondary brain injury.

Preanesthetic evaluation should be as comprehensive as possible but may be limited by the acuity of the clinical situation. In most cases, patients will present to the operating room soon after evaluation and initial management.

Clinical assessment — When time permits, the usual preanesthesia evaluation should be completed, including the details of comorbidities and medications. The patient's neurologic condition may interfere with his or her ability to provide a history.

Rapid neurologic assessment is performed using the Glasgow Coma Scale (GCS) to stratify the severity of TBI, where mild, moderate, and severe TBI are those with GCS scores of 13 to 15, 9 to 12, and <9, respectively (table 1). The severity of TBI estimates the degree of impaired physiology, determines the urgency of a surgical procedure and the plan for postoperative care, and predicts risk for complications and overall prognosis. (See "Traumatic brain injury: Epidemiology, classification, and pathophysiology", section on 'Clinical severity scores'.)

Trauma surgery may be associated with hypotension and a reduction in cerebral perfusion pressure that may lead to secondary brain injury. For nonemergency extracranial surgery, the patient with TBI should be resuscitated and hemodynamically stabilized prior to operative intervention to minimize the chance of intraoperative hypotension. However, recovery of cerebral autoregulation can be delayed for weeks after TBI, particularly in patients with a lower GCS score, diffuse brain injury, and elevated intracranial pressure (ICP) [1]. Patients with delayed recovery of cerebral autoregulation tend to have worse outcomes. (See 'Hemodynamic management' below.)

Preanesthesia evaluation should include a survey of associated injuries. Injuries other than the brain injury (eg, abdominal or orthopedic trauma) may cause significant concealed blood loss, which can result in hypovolemia, anemia, and hypotension with induction of anesthesia.

Laboratory evaluation — Preoperative laboratory tests should be reviewed, including hemoglobin, platelet count, clotting parameters, electrolytes, glucose, and blood gases. A sample should be sent for type and screen (or type and crossmatch if significant blood loss is expected).

Abnormalities of coagulation parameters are common in patients with TBI and require ongoing assessment and correction. (See 'Hemostatic management' below.)

Neuroimaging — Computed tomography (CT) is the preferred imaging modality in the acute phase of TBI, and will detect skull fractures, intracranial hemorrhage, and cerebral edema. Magnetic resonance imaging (MRI) may be used as well. Implications of neuroimaging findings for anesthesia include the following:

●Acute intracranial hemorrhage (ie, subdural hematoma, epidural hematoma) may require emergency evacuation and is often associated with intracranial hypertension. Traumatic subarachnoid hemorrhage may be associated with cerebral vasospasm. (See 'Glucose management' below and "Aneurysmal subarachnoid hemorrhage: Treatment and prognosis", section on 'Vasospasm and delayed cerebral ischemia'.)

●Increased ICP may be evident on neuroimaging even in the absence of hematoma. This is often due to cerebral edema. (See "Management of acute moderate and severe traumatic brain injury", section on 'Neuroimaging'.)

●Skull fracture may be evident on imaging. Care should be taken when handling the head in those with fracture of the outer surface of the cranial vault in order to avoid further brain injury. Those with or at risk of basilar skull fracture should not have objects placed into the nasal cavity (eg, nasotracheal tubes, nasal airways or temperature probes). Also, patients with skull fracture are at increased risk for pneumocephalus and delayed central nervous system infection.

●Chronic intracranial hemorrhage (chronic subdual hematoma) may require either burr-hole evacuation or craniotomy.

ANESTHETIC MANAGEMENT

Goals for anesthetic management — Goals for anesthetic management for patients with TBI include the following:

●Facilitate early cerebral decompression in patients with expanding intracranial hematoma.

●Maintain cerebral perfusion pressure (CPP) and treat increased intracranial pressure (ICP). (See 'Hemodynamic management' below.)

●Avoid secondary insults including hypotension, hypoxemia, hyper- and hypocarbia, hypo- and hyperglycemia, seizures, and coagulopathy. (See 'Hemodynamic management' below and 'Intraoperative ventilation and oxygenation' below and 'Temperature management' below and 'Glucose management' below.)

●Provide adequate analgesia and amnesia.

●Facilitate early postoperative neurologic evaluation when possible.

A summary of the anesthetic considerations based on the Brain Trauma Foundation Guidelines for the Management of Severe Traumatic Brain Injury is shown in a table (table 2).

Monitoring — Standard American Society of Anesthesiologists (ASA) monitors (electrocardiography, noninvasive blood pressure (BP), pulse oximetry, capnography, temperature) are used for any patient having anesthesia (table 3). Additional intraoperative monitoring for patients with TBI includes:

●Arterial catheterization – An arterial catheter should be placed for continuous BP monitoring and to facilitate blood sampling. The transducer should be zeroed at the level of the external auditory meatus to ensure that cerebral perfusion is estimated accurately, especially when the head is elevated above the heart. Importantly, the placement of an arterial catheter should not delay the surgical evacuation of a rapidly expanding intracranial hematoma.

●ICP monitoring – ICP monitors are often placed for patients with TBI. Indications for monitoring and the various types of monitors are discussed separately. (See "Evaluation and management of elevated intracranial pressure in adults", section on 'Types of monitors' and "Management of acute moderate and severe traumatic brain injury", section on 'ICP and CPP monitoring'.)

ICP monitoring should be continued during patient transport to allow for immediate treatment of increased ICP. If a ventriculostomy is being used for ICP measurements, the ventriculostomy catheter should be clamped (ie, closed to the drip chamber of the drainage system but open to continuous transduction) during patient transport to avoid catheter malfunction or dislodgement, or excessive cerebrospinal fluid (CSF) drainage. If ICP increases during transport, iatrogenic causes should be ruled out (eg, transducer positioned too low) and physiologic causes should be corrected (eg, hypotension, hypercapnia, inadequate sedation). If intracranial hypertension persists, CSF drainage can be considered. The stopcock can be adjusted to allow for ICP measurement with or without CSF drainage, though the "true" ICP and waveform are best evaluated with the ventriculostomy at least transiently closed off to drainage [2].

In contrast with arterial or central venous monitoring transducers, ICP monitors should never be connected to a pressure bag; dangerous increase in ICP can occur. Perioperative management of ICP monitors should be discussed with the neurosurgery and intensive care teams.

●Electroencephalography (EEG) monitoring – EEG monitoring may be used in patients with TBI with suspected seizure activity in the ICU. While raw EEG monitoring is impractical intraoperatively, the information about ongoing seizures should be obtained for patients undergoing surgery and antiepileptic medications continued in the perioperative period.

Processed EEG monitoring may be used to guide anesthetic depth when possible for extracranial surgery.

●Advanced neuromonitoring – Novel techniques for advanced, or multimodal, neuromonitoring have been developed but are not in widespread use. These monitors are typically placed in the intensive care unit (ICU). Jugular venous oximetry and brain tissue oxygen (O₂) tension monitoring are more readily used intraoperatively than other techniques, such as transcranial Doppler sonography, cerebral microdialysis, and thermal diffusion flowmetry. (See "Management of acute moderate and severe traumatic brain injury", section on 'Advanced neuromonitoring'.)

•Jugular venous oximetry allows for assessment of cerebral O₂ supply and demand without interfering with the surgical field. Monitoring can be accomplished via co-oximetry or with a fiberoptic cable. Normal jugular venous O₂ saturation (SjvO₂) is 55 to 75 percent. Low SjvO₂ can result from systemic hypotension, systemic hypoxemia, increased ICP, or anemia. SjvO₂ can also be used to effectively titrate hyperventilation as a means to decrease ICP, as high ICP and excessive hyperventilation can both lead to low SjvO₂.

•Brain tissue O₂ tension monitoring allows for determination of the partial pressure of O₂ in brain tissue (PtiO₂). Normal PtiO₂ is 20 to 35 mmHg, and values below 10 to 15 mmHg are associated with poor outcome [3,4]. Factors that lead to a decrease in SjvO₂ can potentially cause a decrease in PtiO₂. One major limitation of this technique is related to the location of the tip of the monitoring probe. The probe is usually placed in white matter by a neurosurgeon. If the probe is located in healthy brain distant from the injury, impaired perfusion and oxygenation of an injured or at-risk brain may not be detected.

When such monitors are in place, perioperative management should be discussed with the neurointensive care staff.

Venous access — Intravenous (IV) access should be tailored to the planned procedure, expected intraoperative blood loss, and estimated preoperative blood loss. Even with isolated TBI, scalp wounds, scalp dissection, and intracranial hemorrhage can result in large-volume blood loss.

Central venous catheters (CVCs) may be needed for patients with TBI for secure venous access and vasopressor administration. However, placement of a CVC should not delay evacuation of a rapidly expanding intracranial hematoma, and it is very uncommon to place these lines prior to cerebral decompression. A CVC may be placed after cerebral decompression for subsequent ICU care, or for patients with TBI who undergo extracranial surgery. The choice of the site for placement of a CVC varies by institution; some centers avoid the internal jugular site for central venous access in patients with acute TBI because of the potential for increasing jugular venous pressure and thereby increasing ICP. Trendelenburg positioning should be avoided or minimized during placement of a CVC in the neck or torso for these patients because the head-down position increases ICP. Subclavian venous access may be preferred over internal jugular in patients with known/possible unstable cervical spine injury.

Choice of anesthetic agents — The anesthetic agents and their doses used to induce and maintain general anesthesia should be chosen to maintain hemodynamic stability, preserve cerebral perfusion, avoid increases in ICP, and avoid secondary brain injury. There are no data demonstrating the association of any specific anesthetic agent with better neurologic outcomes in patients with TBI. However, there may be differences in hemodynamics related to the choice of anesthetics, particularly propofol.

●There is increased interest in perioperative use of ketamine in patients with TBI. In one small randomized trial including 50 patients who required surgery for moderate to severe TBI, induction and maintenance of anesthesia with ketofol (ketamine/propofol admixture) resulted in better hemodynamic stability, lower vasopressor requirement, and similar brain relaxation, compared with induction and maintenance with propofol [5]. Current evidence suggests that ketamine can be used safely for analgesia and sedation in patients with TBI [6].

●In a randomized trial including 42 patients who underwent decompressive hemicraniectomy for severe TBI, use of propofol for maintenance of anesthesia resulted in lower intraoperative mean arterial pressure compared with use of sevoflurane at a similar depth of anesthesia [7]. Jugular venous oximetry and brain relaxation scores were similar in the two groups.

The choice of induction agents and the effects of anesthetic agents on cerebral physiology are discussed in more detail separately. (See "Anesthesia for craniotomy in adults", section on 'Choice of induction agents' and "Anesthesia for craniotomy in adults", section on 'Maintenance of anesthesia' and "Induction of general anesthesia: Overview", section on 'Intravenous anesthetic induction'.)

Our strategy — There are many ways to safely manage anesthesia for patients with TBI. The strategy should be modified based upon individual patient factors and the specific surgery. Our usual approach is as follows:

●Premedication – No premedication preferable for patients with possible intracranial hypertension

●Rapid sequence induction and intubation (RSII)

•Fentanyl 2 to 4 mcg/kg IV

•Lidocaine 1 to 1.5 mg/kg IV

•Propofol 1.5 to 2 mg/kg IV, dose modified for patient factors

•Etomidate 0.2 to 0.6 mg/kg IV may be used in patients hypotensive prior to induction

•Succinylcholine 1 to 1.5 mg/kg; for patients with possible intracranial hypertension, defasciculating dose of nondepolarizing NMBA (eg, rocuronium 2 mg IV, cisatracurium 1.5 mg IV, or vecuronium 0.3 mg IV) followed by succinylcholine 1.5 to 2 mg/kg IV

If succinylcholine is contraindicated, rocuronium 1 mg/kg IV

●Maintenance

•Isoflurane or sevoflurane <1 minimum alveolar concentration (MAC) end-tidal concentration or propofol 70 to 140 mcg/kg/minute (ideally titrated to processed EEG monitoring, when possible)

•Low-dose ketamine (up to 10 mg/hour) or dexmedetomidine (0.2 to 0.6 mcg/kg/hour) may be used as anesthetic adjuncts

•Fentanyl 1 to 2 mcg/kg every one to two hours depending on hemodynamic status (higher in range if neuromuscular blocking agent [NMBA] is not used)

•Rocuronium/vecuronium titrated to one to two twitches in train-of-four (TOF) (if not contraindicated by neuromonitoring)

●Antiemetic – Ondansetron 4 mg IV one hour prior to emergence

●Pain control alternatives (see "Anesthesia for craniotomy in adults", section on 'Emergence from anesthesia')

•Fentanyl, morphine, or hydromorphone titrated to effect postoperatively

Or

•Morphine 3 to 5 mg IV or hydromorphone 0.5 mg IV 30 minutes prior to emergence, further opioid titrated to effect after postoperative neurologic examination

Additionally, acetaminophen 1000 mg IV may be administered to supplement analgesia without compromising neurologic assessment.

Airway management — Many patients with severe TBI come to the operating room with an endotracheal tube in place. For those who require airway management with induction of anesthesia, the following principles apply:

●Cervical spine injury – Unless the cervical spine has been formally cleared, cervical spine injury should be assumed for patients with severe TBI. The reported incidence of cervical spine injury in patients with severe head injury is between 4 and 8 percent; many of these injuries are mechanically unstable and are associated with spinal cord injury [8]. Movement of the cervical spine must be minimized during airway management, to avoid spinal cord injury. Airway management for these patients is discussed separately. (See "Anesthesia for adults with acute spinal cord injury", section on 'Airway management'.)

●Aspiration risk – Patients with TBI should be assumed to have a full stomach, and therefore to be at risk for aspiration of stomach contents. The decision to perform RSII should be based on the predicted difficulty with airway management and other patient factors. (See "Rapid sequence induction and intubation (RSII) for anesthesia" and "Management of the difficult airway for general anesthesia in adults" and "Airway management for induction of general anesthesia", section on 'Creation of a strategy for airway management'.)

●Neuromuscular blocking agents – Neuromuscular blocking agents (NMBAs) are routinely administered after induction of anesthesia to facilitate endotracheal intubation, and during maintenance of anesthesia as required by the surgical procedure. For RSII, either succinylcholine or rocuronium are most commonly used. (See "Clinical use of neuromuscular blocking agents in anesthesia", section on 'Endotracheal intubation' and "Rapid sequence induction and intubation (RSII) for anesthesia", section on 'Neuromuscular blocking agents (NMBAs)'.)

While it is often argued that succinylcholine, a depolarizing NMBA, can produce a transient increase in ICP, possibly the result of an increase in CBF related to the arousal response to muscle fasciculations [9], studies have shown that succinylcholine administered to mechanically ventilated patients with TBI does not cause a significant change in ICP or CPP [10,11]. In addition, the anticipated increase in ICP with succinylcholine can be attenuated by administration of a defasciculating dose of a nondepolarizing NMBA [12] or with an adequate dose of induction agent.

For RSII in patients in whom ICP is a concern, we administer a defasciculating dose of nondepolarizing NMBA (eg, rocuronium 2 mg IV, cisatracurium 1.5 mg IV, or vecuronium 0.3 mg IV) followed by succinylcholine 1.5 to 2 mg/kg IV. For RSII when succinylcholine is contraindicated (eg, burns, denervation injury), we administer rocuronium 1 mg/kg IV.

Hemodynamic management — Hemodynamic management in TBI patients requires judicious use of fluids, blood products, vasopressors, and inotropes. The goal for intraoperative hemodynamic management for patients with TBI is the maintenance of adequate cerebral blood flow (CBF) to avoid secondary injury. Through autoregulation, the normal cerebral vasculature maintains an adequate CBF across a wide range of mean arterial blood pressure (MAP) (see "Evaluation and management of elevated intracranial pressure in adults", section on 'Autoregulation'). However, following TBI, autoregulation of CBF may be impaired or abolished, even in those with mild injury [13-22]; impairment may occur immediately after injury and can persist for up to or beyond two weeks [1]. Patients with impaired cerebral autoregulation are described as "pressure-passive," such that a sudden rise in MAP can lead to secondary hemorrhage, edema, and elevated ICP due to increased cerebral blood volume and hyperemia. Conversely, drops in MAP may be associated with hypoperfusion and ischemia.

Bedside measurement of CBF is not easily obtained. CPP, the difference between the mean arterial pressure (MAP) and the ICP (CPP = MAP – ICP) is a surrogate measure. Episodes of hypotension (low MAP), raised ICP, and/or low CPP are associated with secondary brain injury and worse clinical outcomes [23-25].

Goal intracranial pressure and cerebral perfusion pressure — We agree with the Brain Trauma Foundation guidelines, which recommend maintaining ICP <22 mmHg and a CPP target of 60 to 70 mmHg, avoiding aggressive attempts to achieve a CPP above 70 mmHg [26-28]. Efforts to optimize CPP should first treat intracranial hypertension [29]. Patients with more severely impaired autoregulation in particular may be more likely to respond to efforts to lower ICP than to CPP therapy focused on raising blood pressure [30]. (See "Anesthesia for craniotomy in adults", section on 'Brain relaxation'.)

Goal blood pressure — Avoidance of hypotension in patients with severe TBI is a primary perioperative goal, as observational data suggest that hypotension is associated with poor neurologic outcome in these patients. We agree with the Brain Trauma Foundation guidelines [28] for goal blood pressure as follows:

●Systolic blood pressure (SBP) ≥100 mmHg for patients 50 to 69 years old

●SBP ≥110 mmHg for patients 15 to 49 or >70 years old

Mean arterial pressure and CPP must be considered in addition to SBP. Higher SBP may be required to achieve adequate CPP, particularly in patients with severely increased ICP.

Patients with TBI associated with polytrauma are at risk for hypotension related to blood loss and other organ damage. Low admission GCS score, preoperative tachycardia and hypertension, delayed surgery [31], subdural hematoma (SDH), multiple lesions on computed tomography (CT), and longer duration of anesthesia have all been associated with increased risk of intraoperative hypotension [32]. Sudden hypotension can occur in these patients following removal of the bone flap and dural incision, which is thought to result from sudden decrease in ICP [31,33].

Hypotension during emergency craniotomy for TBI occurs in 32 to 65 percent of adult patients [32,34]. Patients with TBI who suffer intraoperative hypotension following decompressive craniotomy are at increased risk of death, persistent vegetative state, or disability compared with patients without hypotensive episodes [31]. The duration of intraoperative hypotension is inversely correlated with neurologic outcome.

Intraoperative fluid management — Warm, non-glucose-containing isotonic crystalloid solution should be administered to maintain euvolemia for patients with TBI [35-37]. The role of colloids is controversial; we do not use albumin in our TBI patients because of concerns that colloids may increase ICP in patients with altered blood-brain barriers.

The Saline versus Albumin Fluid Evaluation (SAFE) study raised concerns about the use of albumin in patients with TBI. The SAFE study compared the effects of fluid resuscitation with albumin or saline in a heterogeneous group of patients in ICUs, and reported an increase in the death among patients with TBI who received albumin [38]. A post-hoc analysis of the data for patients with TBI found that resuscitation with albumin was associated with higher mortality compared with normal saline (33 versus 20 percent); this risk was even more pronounced in those with severe TBI (42 versus 22 percent) [39]. In a subsequent study that analyzed the 321 TBI patients in the SAFE study who received ICP monitoring, resuscitation with albumin was associated with increased ICP and with associated interventions used to treat increased ICP (ie, sedatives, analgesics, and vasopressors) during the first week after injury [40]. Twice as many patients who received albumin died during that first week compared with those who received saline (34 versus 17 percent). These findings are in accordance with concerns that increased extravasation of albumin from areas of altered blood-brain barrier permeability may lead to increased cerebral interstitial colloid osmotic pressure and increased ICP [41]. The findings from the SAFE study have not been replicated, and it is possible that the relatively hypotonic albumin solution used in the study may have contributed to adverse outcomes. Nonetheless, because of the possibility of increasing cerebral edema with albumin, we avoid albumin in patients with TBI, and instead administer crystalloid and vasoactive medications to support blood pressure.

There are no data to support or refute the use of starch-based colloids in TBI patients. We avoid starches due to similar concerns as with albumin, in addition to the potential for altered coagulation that is associated with the use of starch-based colloids. (See "Intraoperative fluid management", section on 'Hydroxyethyl starches'.)

Electrolyte imbalances are common in patients with TBI and should be assessed regularly intraoperatively, along with other laboratory values.

Administration of hypertonic saline and mannitol as osmotherapy for intracranial hypertension is discussed separately. (See "Anesthesia for craniotomy in adults", section on 'Planned brain relaxation' and "Management of acute moderate and severe traumatic brain injury", section on 'Osmotic therapy'.)

Blood transfusion — The optimal intraoperative transfusion strategy for patients with TBI is uncertain. Anemia can cause secondary brain injury by reducing O₂ delivery to the brain and is associated with worse outcomes [42,43]. However, the available literature on the effects of transfusion on outcomes in patients with TBI does not support the use of liberal transfusion thresholds (ie, a higher goal hemoglobin level). In a randomized trial of 200 patients with moderate or severe TBI, a liberal transfusion threshold (>10 g/dL) did not result in improved outcome at six months compared with a threshold of 7 g/dL, and the 10 g/dL threshold was associated with a higher incidence of adverse thromboembolic events [44].

We do not routinely follow a liberal transfusion strategy (ie, Hgb >10 g/dL) for patients with TBI. This is similar to our approach for other critically ill patients. Transfusion should be based on ongoing bleeding, the clinical status, and patient comorbidities, rather than a specific hemoglobin trigger. (See "Indications and hemoglobin thresholds for RBC transfusion in adults", section on 'Overview of our approach'.)

Tranexamic acid — Administration of the antifibrinolytic tranexamic acid may be indicated in some patients with TBI. Tranexamic acid is typically administered immediately after diagnosis of TBI as an infusion of 1 g IV over 10 minutes, followed by IV infusion of 1 g over 8 hours. Infusion should be continued during anesthesia.

The CRASH-3 trial demonstrated reduced head injury related mortality for patients with mild to moderate TBI who received tranexamic acid within three hours of injury, without an increase in vascular occlusive events or seizures [45]. However, subsequent meta analyses that included the CRASH-3 trial did not find benefit of tranexamic acid on mortality or disability after TBI [46,47]. The CRASH-3 trial and use of tranexamic acid in patients with TBI are discussed in detail separately. (See "Management of acute moderate and severe traumatic brain injury", section on 'Antifibrinolytic therapy'.)

Vasoactive medication — Vasoactive drugs are commonly administered during anesthesia to achieve BP goals. The effects of these drugs on cerebral physiology are complex and reflect the baseline BP, the status of autoregulatory mechanisms, the mechanism of the drug effect, and the magnitude of BP change. Moreover, cardiac dysfunction occurs in patients after moderate to severe TBI. The resulting mild to moderate reduction in left ventricular ejection fraction should be accounted for when selecting vasopressors or inotropes [48,49]. The effects of vasoactive medications on cerebral blood flow in the absence of brain injury are discussed separately. (See "Anesthesia for craniotomy in adults", section on 'Vasoactive drugs'.)

Vasopressors — For patients with TBI, available evidence does not support a preference for a particular vasopressor over others. The selection of vasopressor should be based on patient factors and the clinical situation.

●Phenylephrine – The effect of phenylephrine on CBF is controversial. At least in some circumstances, phenylephrine may be associated with a decrease in cerebral oxygenation. (See "Anesthesia for craniotomy in adults", section on 'Vasoactive drugs'.)

However, phenylephrine may be the most commonly used intraoperative vasopressor infusion and can effectively increase MAP and CPP [50].

●Other vasopressors – Norepinephrine and dopamine have been compared in small randomized trials in patients with TBI. In one study including 20 patients with TBI in an ICU, for the same MAP, ICP was higher with dopamine than with norepinephrine, without a change in CBF [51]. In another study of 10 patients with TBI, there was no difference in CBF or ICP between norepinephrine and dopamine, though norepinephrine produced a more predictable hemodynamic response [52].

Vasodilators — Vasodilators (ie, nitroprusside, nitroglycerin, hydralazine, and calcium channel blockers) dilate the cerebral circulation and can increase CBF, and therefore ICP, if adequate MAP is maintained. Thus, vasodilators should be used with caution in patients with increased ICP.

Beta blockers — Beta blockers either reduce or have no effect on CBF and cerebral metabolic rate (CMR) [53]. Beta blockers have been proposed as a neuroprotective treatment after TBI, though evidence of long-term benefit is lacking [54].

Intraoperative elevated intracranial pressure — If the surgeon encounters cerebral edema during craniotomy, or ICP increases during intracranial or extracranial surgery, we follow a systematic approach to evaluation and treatment, which is discussed more fully separately. (See "Anesthesia for craniotomy in adults", section on 'Intraoperative cerebral edema'.)

Intraoperative ventilation and oxygenation — The goals for oxygenation and ventilation for patients with TBI should be a partial pressure of O₂ (PaO₂) >60 mmHg [55,56], and partial pressure of carbon dioxide (PCO₂) 35 to 38 mmHg, unless therapeutic hyperventilation is required.

●Oxygenation – Hypoxemia is associated with increased mortality and poor neurologic outcome in patients with TBI [57-59]. We agree with the Brain Trauma Foundation recommendation to maintain a PaO₂ >60 mmHg and a peripheral O₂ saturation of >90 percent [55].

Studies of the effect of hyperoxia in these patients are conflicting, with some studies reporting worse outcomes with extreme hyperoxemia [57,58] and others reporting improved outcomes [60,61]. The mechanism by which hyperoxia may be deleterious after TBI is unclear but may involve hyperoxic cerebral vasoconstriction or production of reactive O₂ species. Given the established risk to the brain from hypoxia and concern for injury by hyperoxia, we suggest maintaining a PaO₂ of 60 to 200 mmHg.

●Ventilation – Ventilation should be guided by blood gases rather than by end-tidal CO₂ (ETCO₂). While ETCO₂ generally correlates well with PCO₂, a number of factors (eg, age, lung disease, surgical positioning) can result in significant discrepancy [62,63].

Hypercarbia should always be avoided for patients with TBI since elevations in PCO₂ result in increased CBF and may increase ICP.

Hyperventilation should be used selectively. Hyperventilation and the resulting reduction in CBF may be required to reduce ICP or to improve surgical exposure by relaxing the brain in the setting of cerebral edema. However, the vasoconstriction that accompanies hyperventilation may result in ischemia, particularly for at-risk brain tissue after TBI. Multiple studies using a variety of methodologies have reported evidence of brain ischemia in injured brains with hyperventilation to a PCO₂ of 25 to 30 mmHg [64-66]. Thus, when indicated as part of a multimodal approach to brain relaxation, we hyperventilate to achieve a PCO₂ of 30 to 35 mmHg but limit the duration of hyperventilation. When prolonged hyperventilation is required, cerebral oxygenation should be monitored with jugular venous oximetry or PtiO2, or CBF should be monitored with transcranial Doppler ultrasonography [35-37,67].

A multimodal approach to brain relaxation is discussed separately. (See "Anesthesia for craniotomy in adults", section on 'Brain relaxation'.)

Temperature management — Intraoperative normothermia is the goal for temperature management for most patients with TBI. For patients who are being treated with therapeutic hypothermia preoperatively, therapeutic hypothermia should be continued during anesthesia.

●Fever worsens outcome after stroke and probably severe TBI, presumably by aggravating secondary brain injury, and should be avoided and aggressively treated [23,68].

●Therapeutic hypothermia has not been shown to improve outcome in patients with TBI and may be associated with negative outcomes. Induced hypothermia should be reserved for patients with elevated ICP refractory to other therapies. (See "Management of acute moderate and severe traumatic brain injury", section on 'Hypothermia'.)

Glucose management — Intraoperative hyperglycemia occurs in 15 to 20 percent of patients with TBI requiring craniotomy [69,70]. While both hyper- and hypoglycemia are associated with worse outcome in severe TBI, the optimal goal for blood glucose with TBI is unclear, and tight glycemic control in these patients is controversial. We monitor blood glucose during surgery and aim for a blood glucose between 80 and 140 mg/dL. (See "Management of acute moderate and severe traumatic brain injury", section on 'Glucose management'.)

Antiseizure drugs — Phenytoin is recommended for prevention of early post traumatic seizures in the current Brain Trauma Foundation guidelines for patients with TBI [71]. Based on this recommendation, the author administers phenytoin or fosphenytoin; an advantage to fosphenytoin is that it is not associated with tissue damage with extravasation, unlike phenytoin. Others administer levetiracetam to prevent post traumatic seizures in patients with severe TBI. This issue is discussed separately. (See "Management of acute moderate and severe traumatic brain injury", section on 'Antiseizure medications and electroencephalography monitoring'.)

Anesthesiologists should ensure continuation of scheduled anticonvulsants in the perioperative period while carefully avoiding associated adverse effects, particularly hypotension. (See "Management of acute moderate and severe traumatic brain injury", section on 'Antiseizure medications and electroencephalography monitoring' and "Anesthesia for craniotomy in adults", section on 'Antiseizure drugs'.)

Phenytoin or fosphenytoin must be administered slowly (phenytoin at ≤50 mg/minute) to prevent hypotension and bradycardia. (See "Anesthesia for craniotomy in adults", section on 'Antiseizure drugs'.)

Intraoperative glucocorticoids — Routine administration of glucocorticoids, which are commonly administered during craniotomy for elective neurosurgical procedures, is not recommended for patients with TBI [71,72]; large studies have found that glucocorticoid therapy is harmful for patients with moderate to severe TBI. (See "Management of acute moderate and severe traumatic brain injury", section on 'Glucocorticoids'.)

Hemostatic management — Approximately one-third of patients with severe TBI develop a coagulopathy, which is associated with an increased risk of hemorrhage enlargement, poor neurologic outcomes, and death. (See "Management of acute moderate and severe traumatic brain injury", section on 'Management of coagulopathy'.)

The antifibrinolytic agent tranexamic acid is increasingly administered to control bleeding after trauma and is recommended in some patients with acute TBI. This issue is discussed separately. (See "Management of acute moderate and severe traumatic brain injury", section on 'Antifibrinolytic therapy'.)

Coagulation parameters should be measured during surgery and anesthesia, and abnormalities should be corrected promptly. Recommendations for management of patients with abnormal coagulation parameters unrelated to warfarin are limited by lack of supporting evidence. A reasonable, if somewhat arbitrary, target for therapy is an international normalized ratio (INR) <1.4. However, this target may be difficult to achieve, and efforts to achieve this goal should be guided by the clinical situation. When a coagulopathy is identified, it is reasonable to use FFP, prothrombin complex concentrate (PCC), and/or vitamin K (10 mg IV over 20 to 60 minutes) for warfarin-reversal (see "Management of warfarin-associated bleeding or supratherapeutic INR", section on 'PCC products' and "Management of warfarin-associated bleeding or supratherapeutic INR", section on 'Vitamin K dose, route, formulation'). A retrospective review of reversal of coagulopathy in 220 patients with TBI without warfarin therapy reported that administration of PCC with FFP achieved faster correction of INR compared with FFP alone [73].

Thrombocytopenia and abnormal platelet function are also associated with an increased rate of progression of intracranial hemorrhage. The optimal platelet transfusion trigger has not been determined. In patients with thrombocytopenia, many centers, including ours, choose to maintain a platelet count >75,000/mm³ with platelet transfusions if necessary. If there is clinical evidence of inadequate hemostasis, we increase the goal to 100,000 platelets/mm³.

For patients who are taking antiplatelet medication (ie, aspirin, clopidogrel), the benefits of platelet transfusion with TBI are not clear [74-76]. A small pilot study evaluated the effect of platelet transfusion on platelet function for patients with traumatic intracranial hemorrhage with and without prior aspirin therapy [77]. Trauma-induced platelet dysfunction was found in all patients. Transfusion of one unit of platelets improved aspirin-induced but not trauma-induced platelet dysfunction; the study was too small to assess outcomes.

Neuroprotection — In addition to avoidance of physiologic perturbations that are associated with secondary brain injury (ie, abnormalities in cerebral perfusion pressure, oxygenation, ventilation, temperature and glucose), a wide range of agents targeting various aspects of the TBI injury cascade have been tested in clinical trials. To date, no neuroprotective agents or strategies (including induced hypothermia) have been shown to produce improved outcome. (See "Management of acute moderate and severe traumatic brain injury", section on 'Neuroprotective treatment'.)

EMERGENCE AND TRANSFER OF CARE — Many patients presenting for the evacuation of an epidural hematoma or isolated depressed fracture of the skull can be awoken from anesthesia and extubated at the end of craniotomy. The usual procedures for extubation of patients with difficult intubation or airway concerns should be followed, and are discussed separately. (See "Management of the difficult airway for general anesthesia in adults", section on 'Extubation'.)

Patients with severe TBI, SDH or other intracranial lesions, or polytrauma may remain intubated and transported to the intensive care unit (ICU). An immediate postoperative computed tomography (CT) scan may be required to confirm intracranial decompression and/or to rule out progression of intracranial hemorrhage. All intraoperative monitoring should be continued during transport. A standardized handoff checklist can facilitate safe transfer of care to the ICU staff.

SPECIAL POPULATIONS — Intracranial hemorrhage commonly occurs as a result of traumatic head injury.

Epidural hematoma — Intracranial epidural hematoma is caused by bleeding in the potential space between the dura and the skull, usually as a consequence of arterial bleeding due to traumatic head injury. The epidemiology, clinical manifestations, diagnostic evaluation, and management decisions are discussed separately. (See "Intracranial epidural hematoma in adults".)

Acute symptomatic epidural hematoma is a neurosurgical emergency, requiring decompression to prevent brain herniation and death. Craniotomy with hematoma evacuation is the mainstay of surgical treatment, though in some cases, burr hole evacuation (trephination) may be performed.

Patients who come to the operating room for treatment of epidural hematoma should be managed according to the basic principles outlined above.

Subdural hematoma — Subdural hematomas (SDHs) form between the dura and arachnoid membranes. SDH is most commonly the result of venous bleeding, though arterial rupture accounts for up to 30 percent of cases. Head trauma is the most common cause of SDH; presentation may occur acutely or insidiously with subacute or chronic SDH. SDH can occur following even minor head trauma in older patients taking anticoagulants who have significant cerebral atrophy that leads to stretching of bridging veins. (See "Subdural hematoma in adults: Etiology, clinical features, and diagnosis".)

Acute symptomatic SDH is a neurosurgical emergency that often requires emergency craniotomy, burr hole trephination, or decompressive craniectomy, and often requires general anesthesia.

Patients with chronic SDH may require urgent surgical hematoma evacuation if they develop severe cognitive impairment or progressive neurologic deterioration.

In some cases, chronic SDH is managed conservatively without surgery, even in patients with cognitive impairment, when there is no evidence of intracranial hypertension. For liquified chronic SDH that fails to resolve spontaneously, one or more burr holes may be placed to allow drainage of the hematoma. These procedures may be performed with monitored anesthesia care rather than general anesthesia for many patients.

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Increased intracranial pressure and moderate-to-severe traumatic brain injury".)

SUMMARY AND RECOMMENDATIONS

●Goals – The goal for anesthetic management for patients with traumatic brain injury (TBI) is to avoid secondary brain injury by preventing hypotension, hypoxemia, hypo- or hypercarbia, fever, hypo- or hyperglycemia, and/or increased intracranial pressure (ICP). (See 'Goals for anesthetic management' above.)

●Associated injuries – Patients with TBI may have associated injuries that complicate anesthetic management.

•Cervical spine injury should be assumed for patients with TBI unless explicitly ruled out; movement of the cervical spine must be minimized during airway management. (See 'Airway management' above.)

•Patients with TBI are assumed to have a full stomach and at risk for aspiration of stomach contents with induction of anesthesia. The decision to perform a rapid sequence induction should be based on predicted airway difficulty and patient factors.

•Abdominal and orthopedic injury may conceal blood loss and result in hypovolemia and anemia, which can increase the risk of hypotension with induction of anesthesia.

●Induction – For patients with TBI, we usually perform a rapid sequence induction and intubation (RSII).

●Maintenance

•Choice of anesthetics – We maintain anesthesia with a low-dose inhalation agent and opioids. For patients with potential for increased ICP, total intravenous (IV) anesthesia (TIVA) is a reasonable alternative. (See 'Choice of anesthetic agents' above.)

•Hemodynamic management – The goal for intraoperative hemodynamic management for patients with TBI is the maintenance of adequate cerebral blood flow (CBF) to avoid secondary injury. We aim for intracranial pressure (ICP) <22 mmHg, and cerebral perfusion pressure (CPP) of 60 mmHg to 70 mmHg, avoiding aggressive attempts to achieve a CPP above 70 mmHg. We aim for a systolic blood pressure (SBP) ≥100 mmHg for patients 50 to 69 years old, and ≥110 mmHg for patients 15 to 49 or >70 years old. (See 'Hemodynamic management' above.)

•Intravenous fluids – Warm, non-glucose-containing isotonic crystalloid solution should be administered IV to maintain euvolemia for patients with TBI. We do not routinely follow a liberal transfusion strategy (ie, goal hemoglobin >10 g/dL) for patients with TBI. Rather, transfusion should be based on ongoing bleeding, clinical status, and patient comorbidities. (See 'Intraoperative fluid management' above and 'Blood transfusion' above.)

•Ventilation – We manage oxygenation and ventilation for these patients as follows (see 'Intraoperative ventilation and oxygenation' above):

-We aim to avoid hypoxia and hyperoxia with a goal partial pressure of oxygen (PaO₂) between 60 and 200 mmHg.

-Hypercarbia should always be avoided for patients with TBI.

-Hyperventilation to a partial pressure of carbon dioxide (PCO₂) of 30 to 35 mmHg should be used only when indicated and as briefly as possible. Hyperventilation and the resulting reduction in CBF may be required to reduce ICP but may result in brain ischemia.

•Glucose management – We aim for a blood glucose between 80 and 140 mg/dL to avoid secondary brain injury. (See 'Glucose management' above.)

•Temperature management – Normothermia should be the goal for temperature management. For patients who are being treated with therapeutic hypothermia preoperatively, therapeutic hypothermia should be continued during anesthesia. (See 'Temperature management' above.)

•Monitor coagulation – Approximately one-third of patients with severe TBI develop a coagulopathy, which is associated with poor neurologic outcomes and death. Coagulation parameters should be measured during anesthesia, and abnormalities should be corrected promptly. (See 'Hemostatic management' above.)

●Emergence and extubation – The plan for emergence from anesthesia and extubation depends on the severity of the brain trauma and other associated injuries. (See 'Emergence and transfer of care' above.)

●Intracranial hemorrhage – Intracranial hemorrhage commonly occurs as a result of TBI. Epidural hematoma and acute symptomatic subdural hematomas (SDHs) are neurosurgical emergencies that require decompression to avoid brain herniation and death. In most cases, general anesthesia is administered for these procedures. (See 'Special populations' above.)

Subacute and chronic SDH are sometimes drained with burr hole trephination; these cases may often be performed with monitored anesthesia care.

ACKNOWLEDGMENT — The editorial staff at UpToDate acknowledge Pratik V Patel, MD, who contributed to an earlier version of this topic review.