Chapter 35: The Neurocritical Care Airway

Yes, for several reasons. He is in a period of acute neurologic decline, with an inadequate airway to provide for oxygenation and ventilation. He has dangerously dulled airway protective reflexes and could have a full stomach, putting him at risk for large-volume gastric aspiration. He will require an urgent invasive procedure (ventriculostomy placement), will be transported between units, and will undergo further imaging studies, requiring flat positioning on the bed. All of these factors suggest he should be intubated. Of interest is that a patient with the same neurologic examination can sometimes be safely extubated in the recovery period—safely monitored in an ICU, with no procedures or transfers planned, an empty stomach, and no clinical decline anticipated.

Neurocritical care patients include trauma victims with facial or cervical spinal injuries and patients in whom bleeding, seizures, or anatomic complications may cause progression from a state of relative stability to brain herniation and/or cardiopulmonary arrest in a matter of minutes. Furthermore, hypoxemia, hypoventilation, and hyperventilation are all powerful mediators of cerebral blood flow and tissue perfusion, so maintenance of a state of respiratory homeostasis is critical to preventing secondary brain injury.

Finally, aspiration before or during intubation can lead to fever, pneumonia, acute respiratory distress syndrome, and systemic inflammation, each associated with worse neurologic outcomes and increased mortality rate. These concerns, which suggest that intubation may be required for many acutely ill neurology patients, are balanced by the principles of preserving an accurate neurologic examination and avoiding the complications of intubation whenever possible.

Indications for endotracheal intubation in the neurocritically ill are often categorized according to three general criteria¹:

1. Failure to maintain or protect the airway

2. Failure of oxygenation or ventilation

3. An anticipated course of clinical deterioration

These principles are discussed further below.

Is it appropriate to intubate every patient with abnormal airway protection? No, although in the acute phase of a neurologic injury, endotracheal intubation is often indicated and may be lifesaving. Airway protection is a matter of some controversy, in part because of its complexity. A normal airway protective mechanism involves:

1. Coordinated oropharyngeal sensory and muscle activity to move oral secretions, liquids, or food in a posterior and inferior direction (away from the larynx) into the upper esophagus, and the rapid activation of esophageal peristalsis to clear the oropharynx

2. A tight lower esophageal sphincter and low gastric pH

3. Elevation and anterior displacement of the glottis during swallowing, with tight closure and approximation of vocal cords and folds

4. A robust sensory response to solids and liquids at the glottis and lower airways, as well as intact cough centers and efferent nervous pathways to the effector muscles

5. Adequate respiratory muscle strength and tidal volume to generate a strong cough

6. Healthy bronchial epithelium with intact villi that clear foreign substances from the smaller, distal airways

7. Maintaining the airway open during airflow—an active, not passive, process involving pharyngeal dilator muscles

Many patients have impaired execution of these multifold functions but, because of circumstances or redundancy in the system, do not require artificial airways. Nonetheless, patients with incomplete or failed airway protective mechanisms are at high risk of aspirating food, secretions, and gastric contents. A clinically unstable patient with severely impaired airway protection requires intubation, while a clinically stable patient with severely impaired airway protection can often be managed with careful feeding (often through a tube) and high-quality nursing, speech-language pathology, and respiratory care.

Routinely applied airway assessment measures include the Glasgow Coma Scale (GCS) score, strength of cough, quantity and character of oral and respiratory secretions, and an evaluation of oropharyngeal coordination and sensation. An airway protection score has been proposed (Table 35-1).^{2, 3} Assessment of the gag reflex is routine but does not correlate well with laryngeal closure and airway protection^{4, 5}; the gag reflex may be absent in up to 37% of healthy subjects.⁶

In the acute setting, a GCS score less than or equal to 8 has been described as both sensitive and specific for predicting the need for endotracheal intubation,⁷ applied not only in trauma but also in patients with stroke, intoxication, and other etiologies of altered mental status.¹ Several studies have demonstrated that patients with GCS less than or equal to 8 commonly have airway obstruction, hypoxemia, and hypoventilation,⁸ resulting from pooled secretions, anatomic compression, or foreign-body aspiration. While the GCS is routinely employed in the emergency department and by emergency medical services (EMS) as part of a triage process to assess patients for intubation, the GCS was not developed for this purpose and does not address any of the primary issues related to airway protection—cough, the ability to manage secretions in the upper airway, or the acuity or anticipated course of the primary neurologic process. In the ICU, a more sophisticated assessment of the airway is expected, should take into account all of the issues discussed above, and be balanced by the known repercussions of endotracheal intubation: confounding of the neurologic examination, an increased need for neuromonitoring and imaging, a need for vasopressors or fluids to counteract the vasodilatory properties of sedation and analgesia, and ventilator-associated pneumonia.

It is sometimes simple to identify oxygenation or ventilatory failure, such as when a brainstem or spinal cord injury completely eliminates respiratory efforts, when a patient struggles unsuccessfully to breathe against an excessive workload, or when the oxyhemoglobin saturation cannot be maintained despite high inspired oxygen fraction (FIO₂). Other forms of respiratory failure are more subtle, however. Mild hypoventilation and hypercarbia that would be well tolerated in a patient with simple chronic obstructive pulmonary disease exacerbation may lead rapidly to an intracranial pressure (ICP) crisis in a patient with intracerebral hemorrhage or hydrocephalus. Similarly, modestly increased work of breathing that would ordinarily be well tolerated might compromise the ischemic penumbra of a stroke patient with heart failure. In these cases, critical care of the neurologically ill differs significantly from other patients. The neurointensivist must at all times recall that oxygen and carbon dioxide tensions in the cerebral vasculature are potent mediators of blood flow, ICP, and secondary neurologic injury.

Arterial blood gases should be measured in patients with a poor level of arousal, on mechanical ventilation, with significant or suspected respiratory compromise, or with elevated ICP. When cerebral blood flow is jeopardized, when there is elevated ICP or poor intracranial compliance, or when a procedure that jeopardizes ventilation, such as bronchoscopy or tracheostomy, is performed, we recommend continuous capnography and a dynamic assessment of the effects of arterial carbon dioxide and oxygen levels on brain perfusion and ischemia.

It is difficult to provide 100% oxygen to a patient without an endotracheal or tracheostomy tube in place. Oxygen supplementation depends on a variety of factors including the percent oxygen provided, flow rate through the tubing and mask of the device, minute ventilation of the patient, and admixture of room air through leaks in the system or in the upper airways. Commonly employed oxygen delivery devices and their estimated oxygen delivery are described in Table 35-2.

Acute hypoxemic respiratory failure is defined as failure to maintain a partial pressure of arterial oxygen (PaO₂) at 60 mm Hg despite the administration of maximal supplemental oxygen. While these low oxygen levels are usually well tolerated in patients with normal brains, there is reason to view this definition and standard of care with suspicion when brain injury or perfusion is a concern. In traumatic brain injury (TBI), hypoxia (defined as an oxygen saturation as measured by pulse oximetry [SpO₂] ≤ 90%), with a median duration of only 11.5 to 20 minutes, is an independent predictor of mortality.⁹ Low brain tissue oxygen (PbtO₂) is associated with brain ischemia and poor neurologic outcome in TBI.^{10, 11} In healthy individuals, autoregulation of cerebral blood flow maintains oxygenation by shunting blood into ischemic regions to maintain a constant PaO₂, but in the injured brain, this mechanism is frequently absent.

Oxygen delivery within an ischemic region is already marginal, and tolerating borderline blood oxygen may increase cerebral infarction size or worsen hypoperfusion in a brain with ischemia due to ICP crisis. Furthermore, and against classical teaching regarding oxygen delivery, there is some evidence to suggest that brain tissue oxygen levels can be significantly increased by increasing the dissolved partial pressure of oxygen in blood, even when oxyhemoglobin is fully saturated.¹² The Brain Trauma Foundation (BTF) guidelines state “oxygenation should be monitored and hypoxia (PaO₂ < 60 mm Hg or O₂ saturation < 90%) avoided” (level III).¹³ The American Stroke Association recommends maintaining oxygen saturation levels greater than or equal to 95% in acute ischemic stroke (level V).¹⁴

Hypoventilation and hypercarbia in a patient with acute brain injury and elevated ICP constitute an emergency, and failure to provide adequate ventilation may result in vasodilation, increased cerebral blood volume, increased ICP, central downward brain herniation, and death. Conversely, iatrogenic hyperventilation can result in a dramatic increase in the volume of ischemic brain,¹⁵ and even the auto-hyperventilation seen in many brain injuries has recently been associated with decreased PbtO₂.¹⁶ Clinicians should attempt to maintain adequate but not excessive ventilation, and should be aware of the effects of changes in ventilation on brain perfusion and ICP in real time.

The major concerns during intubation are the successful placement of the airway device; avoidance of large-volume aspiration; maintenance of hemodynamic, respiratory, and metabolic homeostasis; management of intracranial pressure; and protection of the cervical spine.

Preparation for intubation in the neurology ICU routinely includes:

1. Assessment of the airway and review of existing records describing the airway

2. Decompression of the stomach, if appropriate

3. Consideration of cervical spinal injury, and a plan to minimize spinal manipulation accordingly (see below)

4. Consideration of intracranial pressure, and a plan to minimize ICP and cerebral perfusion pressure (CPP) fluctuations during laryngoscopy, endotracheal tube (ETT) placement, and the administration of vasodilator medications

5. SpO₂, blood pressure, and ICP monitoring, and potentially capnography

6. Assembly of routine airway equipment, special equipment, and suction

7. Careful consideration of intubating medications to provide excellent sedation, analgesia, amnesia, and muscle relaxation without introducing hypotension, hypoxemia, or ICP crisis

8. Establishment of adequate intravenous access for medications, fluids, and vasopressors if necessary

9. Proper positioning of the patient

10. Determination, based on risk to the patient, of whether the intubation will be performed by a trainee or by the most experienced person present

Patients with intracranial hypertension are at risk for both ICP crisis and critically low CPP during intubation. Clinicians should pay special attention to the adequacy of sedation and analgesia during laryngoscopy, to head-of-the-bed positioning, and to the maintenance of adequate blood pressure and oxygenation during intubation of these patients.

Direct laryngoscopy is a noxious stimulus that causes sympathetic stimulation, potentially triggering tachycardia, hypertension, bronchospasm, and increased ICP.¹⁷ A crucial starting point to controlling ICP is to leave the head of the bed up 30 to 45 degrees during preparation for intubation, and lay the patient flat only during the procedure, then immediately return the bed to its elevated position. If necessary, the patient can be placed in reverse Trendelenburg positioning throughout the intubation. Medications that blunt the ICP rise associated with laryngoscopy are discussed in more detail below.

Hypotension, hypoxemia, and hypercarbia cause vasodilation and an increase in cerebral blood volume, leading to a rise in ICP. Preoxygenation is vital, as it washes out nitrogen in the lungs and prolongs the time to oxyhemoglobin desaturation. The patient's minute ventilation should be maintained throughout the procedure to avoid CO₂ retention—a matter of urgency in patients with central nervous system mass lesions.¹⁸ Adequate intravenous access is critically important to managing hemodynamic changes during intubation, and we suggest routine infusion of isotonic crystalloid during the procedure. Vasopressors should be readily available in the event of hypotension to maintain adequate CPP.

Intubation can be performed under sedation assistance (absence of neuromuscular blockade) or rapid sequence (coadministration of neuromuscular blockade and sedatives) (Table 35-3). Rapid-sequence intubation is suggested when the stomach may be full to minimize the risk of distending the stomach with air, triggering vomiting and gastric aspiration.

Fentanyl has a rapid onset and short duration of action and reduces the hypertensive response to laryngoscopy.¹⁹ Because it suppresses the sympathetic response to hypotension, caution must be used in shock states or hypovolemia. Fentanyl derivatives such as remifentanil, sufentanil, and alfentanil are increasingly utilized worldwide and may be more efficacious in blunting the tachycardic response.¹⁷

Lidocaine at a dose of 1.5 mg/kg intravenously blunts ICP rise during laryngoscopy by reducing tachycardia, airway hyperactivity, cerebral blood flow, cerebral vascular resistance, and cerebral metabolism.²⁰ It can, however, also decrease mean arterial pressure (MAP) and CPP.^{21, 22} The use of lidocaine to reduce ICP during intubation is controversial,^{19, 23} but has been shown to be effective in patients with cerebral neoplasms,²⁴ closed head injuries,²⁵ and known elevated ICPs.²⁶ Its side-effect profile includes hypotension, a decreased seizure threshold, and a low incidence of ventricular tachy-arrhythmias.²⁷

Pretreatment with low-dose nondepolarizing neuromuscular blocking agents prior to the administration of succinylcholine is often recommended in order to prevent fasciculation and ICP rise.^{28, 29, 30} This practice may be effective, but it is not supported by published data.^{17, 31}

Etomidate is one of the most commonly used medications for facilitating endotracheal intubation,³² with powerful sedative and muscle relaxant properties. It is a γ-aminobutyric acid (GABA) agonist without analgesic properties. Etomidate is popular because of its hemodynamically neutral effects and a tendency to reduce ICP and cerebral oxygen demand while purportedly preserving CPP.^{32, 33, 34} Side effects include increases in airway resistance, myoclonus, nausea, and vomiting; reduction of the seizure threshold; and adrenal insufficiency. The clinical sequelae of this well-described adrenal insufficiency are unknown; there is growing concern about the use of etomidate in septic patients, in whom an increased mortality rate has been observed.^{35, 36}

Propofol is a GABA agonist that delivers sedation and anesthesia but not analgesia. It reduces airway resistance, has anticonvulsive and antiemetic effects, and suppresses sympathetic activity. This includes a reduction in cardiac inotropy, systemic vascular resistance, intracranial pressure (by decreasing cerebral blood flow), cerebral blood volume, and cerebral metabolism.³⁷ Propofol provides deeper anesthesia than etomidate and creates intubating conditions similar to succinylcholine when used with a nondepolarizing neuromuscular blocker or opiate.¹⁷ However, propofol causes a reduction in systolic blood pressure by 15% to 33%.³⁸ Extreme caution should be exercised when using propofol as an induction agent in patients who require a higher cerebral perfusion pressure and those patients with known cardiomyopathy or low ejection fraction.

Thiopental causes sedation and amnesia through its GABA-agonist properties. It decreases cerebral blood flow, cerebral metabolism, cardiovascular contractility, systemic vascular resistance, and venous return to the heart. Major side effects include hypotension, allergic reactions (2%), laryngo-spasm, bronchospasm, hypersalivation, and immune suppression.

Ketamine is a “dissociative” anesthetic that provides sedation, amnesia, and analgesia. It is an appealing agent in critical illness because it does not cause vasodilation or hypotension. Ketamine binds to catecholamine receptors, causing an increase in heart rate, cardiac output, contractility, mean arterial pressure, and cerebral blood flow.³⁹ Prior studies have demonstrated that ketamine increases ICP,^{40, 41,42, 43, 44, 45} and some authors have recommended against its use in patients with intracranial hypertension. This recommendation is probably obsolete, however, as improvements in CPP have been clearly demonstrated despite elevated ICP when ketamine was used in conjunction with a GABA agonist.^{46, 47, 48, 49} Clinicians should be aware of the potential for dangerous agitation with ketamine when it is given with inadequate sedation, and that it has been poorly studied in the neurocritically ill.

Neuromuscular blocking agents cause profound skeletal muscle relaxation, creating ideal intubating conditions, and have hemodynamically neutral effects. They are always employed in conjunction with sedation. Succinylcholine is a depolarizing agent that activates the acetylcholine receptor, resulting in defasciculation and transient skeletal muscle paralysis. It has the shortest onset and duration of action (typically < 5 minutes) of all the neuromuscular blockers. Side effects include hyperkalemia, myalgias, and rarely malignant hyperthermia in genetically susceptible patients. Some studies suggest that succinylcholine increases intracranial pressure,⁵⁰ but this has been disputed.^{31, 51} The effect of succinylcholine on ICP is transient and of questionable significance^{17, 52} and should not preclude its use when needed.

Neurocritically ill patients may be at higher risk for succinylcholine-induced hyperkalemia.^{53, 54,55} Conditions leading to an upregulation of acetylcholine receptors cause greater potassium efflux from myocytes with nerve depolarization. This includes patients with disuse atrophy, such as stroke or TBI patients with a sudden onset of weakness or paralysis, occurring after as little as 24 to 72 hours of immobility, and patients with upper or lower motor neuron defects.⁵⁶ This risk may be averted by “precurization”—administration of a small dose of nondepolarizing neuromuscular blockers a few minutes before the succinylcholine—or by simply using a nondepolarizing agent instead.

Take care not to inflate the stomach during bag-mask ventilation (BMV). When appropriate, nasogastric decompression of the stomach should be performed prior to intubation, although a nasogastric tube may make mask ventilation more difficult. Downward cricoid pressure was described in 1961 as resulting in occlusion of the esophageal lumen posteriorly against the vertebral column⁵⁷ and is routinely applied during BMV and rapid-sequence intubation to help prevent the instillation of air into the stomach and regurgitation of gastric contents. Recent data suggest that the technique actually compresses the postcricoid hypopharynx, not the esophagus.⁵⁸ Although limited data confirm that the maneuver actually reduces the risk of aspiration,^{59, 60, 61, 62, 63, 64} cricoid pressure is typically well tolerated, may be helpful, and is unlikely to cause harm. It should not be applied when the cervical spine is unstable, and its use should be terminated if there is difficulty with mask ventilation, airway visualization, or active vomiting.

Because both hypoxemia and hypercarbia often result in secondary brain injury, early recognition of a potentially difficult airway or difficult BMV is critically important. Difficult BMV is more dangerous than difficult intubation, since a patient who is difficult to intubate can typically be maintained indefinitely by BMV. When a difficult airway is identified, it is always appropriate to seek the most expert help available to perform the intubation or provide “backup” for the intubator. Important techniques for managing difficult airways include the use of special equipment designed to facilitate placement of the ETT, placement of temporizing airway devices, and surgical airways. Factors identified as predictive of difficult mask ventilation and difficult airway are listed in Tables 35-4 and 35-5.

Clinicians frequently performing endotracheal intubation should develop true expertise with a modest number of intubating techniques and airway adjunct devices. Commonly employed techniques include bimanual laryngoscopy, videoscopic laryngoscopy, blind intubation using a light wand or intubating stylet, and fiberoptic intubation. Airway adjunct devices are multifold but include the gum elastic “bougie” or Eschmann stylet, light wands, articulating laryngoscope blades, intubating laryngeal mask airways, retrograde intubation kits, and an assortment of videoscopes. In particular, the GlideScope has been shown to increase the success rate of endotracheal intubation among untrained personnel when compared to direct laryngoscopy with a Macintosh blade (success rate 93% versus 51%; P < .01).⁶⁵ Airway adjuncts are summarized in Table 35-6.

“Temporizing” supraglottic devices can be inserted if the airway cannot be intubated or to oxygenate and ventilate while preparations are made for intubation. The most common device is the laryngeal mask airway (LMA), an inflatable latex mask placed blindly into the hypopharynx. While not considered a permanent or “definitive” airway as it does not protect against aspiration, the device requires minimal experience to competently employ and may be extremely helpful if a skilled intubator is not available, if the airway is difficult, or if a beard or facial anomaly makes BMV difficult.

A true emergency arises when a patient cannot be intubated or ventilated. In this situation, an immediate surgical airway may be necessary. A needle, wire-guided, or surgical cricothyrotomy should be performed. Tracheostomy is a more complex and time-consuming procedure and should be reserved for nonemergent situations (see Chapter 39).

Any patient with a confirmed or suspected unstable cervical spine needs to be immediately and carefully placed in a rigid cervical collar or other stabilization device. Manual in-line axial stabilization and gentle traction of the head and neck by an assistant are mandatory if the patient requires any manipulation of the head or neck. During airway management, cervical subluxation occurs during chin lift, jaw thrust, BMV, and tracheal intubation,^{66, 67} as well as maneuvers such as cricoid pressure and head turning. Mask ventilation was found in one study to cause more cervical spine displacement than any method used for tracheal intubation.⁶⁸

If direct laryngoscopy is employed, the cervical collar must be removed for intubation, as greater subluxation occurs with a collar in place than with in-line stabilization. Laryngeal visualization is also improved after the cervical collar is removed.^{69, 70} The collar should be carefully reapplied immediately following intubation.

In-line stabilization places the patient's head and neck into neutral position. Unfortunately, no accepted definition of this ideal position exists.⁷¹ One study demonstrated that a mean of 4 cm of occiput elevation off the bed was required to assume a position as if someone was standing looking straight ahead.⁷² A magnetic resonance imaging study determined that occiput elevation of at least 2 cm was required to maximize the spinal canal/spinal cord ratio at C5 and C6.⁷³ To perform in-line cervical stabilization, the patient is supine with the head and neck in neutral position. With the assistant at the head of the bed, each mastoid process is grabbed with the fingertips and the occiput is cradled in the palms. With the assistant at the side of the bed, stabilization can be provided by cradling the mastoids in the palms and grasping the occiput with the fingertips.⁷⁴

Cricoid pressure causes cervical spine displacement in cadaver studies.⁷⁵ Without posterior support, cricoid pressure is associated with a mean neck displacement of 4.6 mm (range 0-8 mm).⁷⁶ Consequently, if cricoid pressure is necessary for intubation, it must be performed bimanually, with concomitant posterior support of the neck.⁷⁷ This modification should also be applied with the BURP (backward-upward-rightward pressure) maneuver. Many of the same rescue techniques used for a difficult airway are applied during a difficult intubation in a patient with cervical spine injury (see Figures 35-1 and 35-2).

Because the least amount of cervical spine motion detected fluoroscopically after a midcervical spine injury is with fiberoptic nasal intubation,⁶⁶ this approach may be preferable when severe cervical instability is suspected and when time and expertise are available to perform the intubation accordingly.

Traditional weaning parameters such as respiratory rate, tidal volume, rapid shallow breathing index, minute ventilation, negative inspiratory force, and the PaO₂-to-FIO₂ ratio do not predict successful extubation in the neurocritically ill,^{78, 79} probably because the patients often do not have respiratory failure—most are better characterized as having airway failure. Clinicians anticipating extubation are repeatedly faced with the difficult task of predicting the ability of an intubated patient to protect his or her airway. Moreover, it is rare for these patients to rapidly normalize their airway protective reflexes—most will recover to some degree but remain at high risk for aspiration for a variable period of time following extubation.

There are a few reasonable approaches to this problem. The first, supported by a large, single-center observational trial in which patients that were extubated despite low GCS scores had significantly lower mortality rate,² is to attempt extubation once the patient meets traditional weaning criteria. These patients should be:

1. In the recovery phase of the acute illness

2. In an environment where good-quality nursing and respiratory care is performed

3. Without copious secretions

4. Able to mount a vigorous cough

The second is to perform early tracheostomy and percutaneous feeding tube placement. This approach removes the uncertainty of determining when the airway is safe and offers the advantages of allowing for minimization of sedation,⁸⁰ early disconnection from the ventilator, increased ability to perform physical and occupational therapy, and protection against large-volume aspiration. Early tracheostomy delivers multiple advantages for severely injured patients, but those who have a faster recovery than anticipated may undergo unnecessary procedures, accruing the risks of those procedures without any benefit. A third, commonly practiced approach is to perform tracheostomy only after a failed trial of extubation. In the absence of compelling evidence of superiority of one of these approaches, most clinicians practice a combination of them, based on patient- and institution-specific factors.

Postextubation laryngeal edema is a feared cause of reintubation, and a cuff-leak test prior to extubation may predict laryngeal edema and postextubation stridor.^{81, 82, 83, 84, 85, 86} Although overly aggressive administration of the cuff-leak test may lead to unnecessary delays in extubation, a meta-analysis of 14 randomized trials suggested lower rates of reintubation when corticosteroids were administered prior to extubation.⁸⁷ As such, it is reasonable to use the prophylactic administration of corticosteroids 12 hours prior to extubation in patients who fail a cuff-leak test or are suspected for other reasons of having laryngeal edema. While the presence of cuff leak (on patients who previously had cuff leak) may be a reassuring sign, absence of cuff leak is not an absolute contraindication for extubation.

Aspiration associated with brain injury is predicted by a “wet” voice after swallowing liquids, incomplete oral-labial closure, and a high National Institute of Health Stroke Scale score.¹⁴ Up to 70% of stroke patients aspirate as evidenced by videofluoroscopic swallowing studies,^{88, 89} more than half of whom aspirate silently (subglottic penetration of a bolus without elicitation of a cough reflex).⁹⁰ This leads to a sevenfold risk of aspiration pneumonia in stroke patients who aspirate compared to those who do not, and a sixfold greater risk in those with silent aspiration compared to those who cough with aspiration.⁹⁰ Aspiration pneumonia due to dysphagia is a leading cause of death in patients with neurologic disorders.⁹¹ It is therefore imperative to assess a patient's ability to swallow following extubation prior to any oral intake, and to tailor the patient's diet and feeding accordingly.

Airway management in patients with acute brain injury offers unique challenges, and a cautious, thoughtful clinical approach is necessary to minimize harm. Clinicians who approach the neurocritical care airway with respect, consistency, and meticulous preparedness will minimize secondary brain injury and provide their patients with the greatest chance of a good neurologic recovery.