Advanced airway management in the field is an inherently risky procedure, and every effort must be made to maximize first-pass success. Although it is clear that some patients require immediate
endotracheal intubation in the field, this population is not well defined. Advanced airway management comes at the expense of prolonged transport times and may delay definitive in-hospital care, which adversely impacts patient outcomes. Conversely, failure of the patient to protect their own airway, persistent hypoxia despite supplemental oxygen administration, and CO₂ retention are all indications for advanced airway intervention.

Paralytic-assisted endotracheal intubation in the field should only be performed by skilled practitioners practicing in a system with a rigorous quality assurance program and continuous provider training. In systems with short transport times and in patients in whom an oxygen saturation > 90% can be maintained with supplemental oxygen, definitive airway management should be delayed until arrival in the ED. All advanced airway placement should be confirmed with quantitative end-tidal capnography (ETCO₂), which dramatically improves the detection of improperly placed airway devices and inadvertent hyperventilation by field providers.

Avoiding hypotension, and managing it when and if it does occur, is a critical element of the prehospital treatment of the head-injured patient.¹ As MAP falls, CPP follows, predisposing to tissue ischemia. Blood pressure should be monitored as frequently as possible with the most advanced means available.²

Although the concept of prehospital permissive hypotension may be beneficial in some trauma patients, it is detrimental in the setting of brain injury.¹ Hypotension should be immediately identified and aggressively managed. Any ongoing external hemorrhage should be expeditiously addressed and controlled. Scalp lacerations may bleed a large volume into a bulky dressing, and a less bulky dressing should be used with firm constant manual pressure applied to avoid excessive blood loss. Fluid resuscitation should be administered on the basis of local prehospital protocols, but generally consists of crystalloids. Hypertonic saline (HTS) has been suggested as a useful resuscitation solution for patients with TBI in the field, but clinical trials have consistently failed to show any benefit over standard resuscitation with crystalloid solution.^3,4

Severely head-injured patients may present agitated or combative. Transporting a patient in this condition is challenging, and may be unsafe for both patient and providers. Transporting an agitated patient who is fighting against physical restraints may exacerbate physical injury, cause an increase in ICP, and interfere with stabilization and management. The priority of the field provider mirrors that of in-hospital management, including rapidly identifying alternative etiologies of agitation such as hypoglycemia, hypoxia, or hypotension.

Options for management in the field may be limited, and will be based on local emergency medical service (EMS) protocols. Ketamine has a fast onset of action when administered by the intramuscular (IM) route, and may be a viable option for rapid sedation of the agitated patient if available to prehospital providers.⁵ Concerns about neurotoxicity and transient increases in ICP following administration have historically limited its use in TBI, although recent studies have not demonstrated any harm when used as an induction agent.⁶ Benzodiazepines including midazolam are also effective in the rapid sedation of an agitated patient, but the patient must be closely monitored for hypoventilation, hypoxia, and hypotension. Antipsychotics including droperidol, haloperidol, or olanzapine are infrequently carried by prehospital providers, but may be additional considerations if available.^7,8

In the setting of TBI, primary airway injury may result from concomitant craniofacial trauma or neck trauma, bleeding, or vomiting. Secondary airway compromise may be caused by loss of brainstem reflexes, or may result from agitation, hypotension, or mental status changes limiting the patient’s ability to protect their airway. In the setting of existing or anticipated airway compromise,
the airway should be secured early to prevent secondary injury from hypoxia or hypoventilation. A brief neurologic examination should be conducted before advanced airway management with sedation or paralysis.

Before endotracheal intubation, the patient should be preoxygenated to avoid hypoxia during the intubation attempt. Volume resuscitation is paramount to avoid hypotension during intubation, especially when giving medications that may blunt sympathetic drive and its compensatory effect on blood pressure. If there is concern that the patient might become hypotensive during or immediately after intubation, vasopressors either as a drip or in push-dose should be administered before or during the intubation attempt.

Supraglottic stimulation during airway manipulation leads to a release of systemic catecholamines, resulting in a transient increase in ICP. Lidocaine to blunt this response or a defasciculating dose of succinylcholine have shown no benefit in patient-centered outcomes and are no longer recommended. Administration of a short-acting opioid, such as fentanyl at a dose of 3 mcg/kg, may blunt the sympathetic reflex and should be considered, but any benefit must be balanced against risks of hypotension.

RSI is safe and effective in the emergent setting, decreasing the risk of aspiration and increasing the likelihood of first pass success. Although research studies have not demonstrated a clear benefit of RSI over other techniques in terms of outcomes, it remains the preferred method of airway management in the patient with TBI. Etomidate (0.3 mg/kg) is the drug of choice owing to its hemodynamic stability. Ketamine (1-2 mg/kg) is an alternative, especially in a hypotensive patient. Although the use of ketamine in TBI has historically been controversial because of a purported transient increase in ICP after ketamine administration, it is generally considered safe and effective for this indication.^15,16 Rocuronium (1.2 mg/kg) is a nondepolarizing agent and as such does not cause the fasciculations and corresponding rise in ICP seen with the depolarizing agents. However, its duration of action can exceed 1 hour, making repeat neurologic assessments challenging. As such, succinylcholine (1.5 mg/kg) is the drug of choice for paralysis in patients with TBI. Rocuronium would be a second-line agent for those with contraindications to succinylcholine.

Following intubation, ventilation parameters should be carefully controlled and eucapnia meticulously maintained. The partial pressure of arterial carbon dioxide (PaCO₂) is a potent regulator of cerebral arteriolar diameter, impacting ICP and in turn CBF. (see Figure 12.2). Reductions in PaCO₂ cause reflex vasoconstriction throughout the brain, whereas hypercapnia results in vasodilatation. Although hyperventilation decreases ICP, the corresponding decrease in cerebral perfusion leads to worse patient outcomes. Unfortunately, unintentional hyperventilation during manual ventilation following intubation is common, underscoring the importance of using quantitative ETCO₂. Although hypocapnia may be deleterious, hypercarbia (PaCO₂ > 45 mm Hg) has also been associated with increased hospital mortality and should similarly be avoided.