Airway management is frequently necessary for patients with neurologic injury or disease. The principles of airway management in neurologic patients are fundamentally the same as in all other critically ill patients—obtain a secure conduit to facilitate gas exchange in as safe a manner as possible. Neurologic patients require intubation for a variety of reasons, most of which are like other critically ill patient populations. Broadly, these relate to airway protection (depressed level of consciousness, aspiration, or to facilitate imaging, procedures, and treatments) or correcting defective gas exchange (hypoxemia, hypercapnia).

There is a history of approaching the intubation of neurologic patients differently, often with complicated pharmacologic cocktails such as high-dose fentanyl and lidocaine prior to induction. While different approaches may be warranted for certain neurologic patients and will be discussed here, these are based on largely physiologic or mechanistic grounds rather than patient outcomes data. Evidence to support modification of the usual airway strategies for neurologic patients is limited and largely derived from theory or, at best, observational data. Such nuances and pretreatment regimens increase complexity and task loading. The fundamentals of safe airway management discussed throughout this book that apply to all patients also apply to neurologic patients and should be the priority to prevent complications.

The most important nuance with intubation in most neurologically injured patients relative to other types of critical illness is their susceptibility to secondary brain injury. The primary brain injury is the initial insult—such as an ischemic stroke, intraparenchymal hemorrhage, or brain trauma, and has typically already occurred. Secondary brain injury happens when physiologic conditions conspire to potentiate or cause ongoing brain injury. The most common physiologic conditions leading to secondary brain injury are hypoxemia, hypotension, and hypercapnia—all conditions directly related to and affected by airway management. These physiologic parameters have an outsized effect on brain tissue oxygen delivery because the injured brain suffers from impaired autoregulation. The mechanisms that typically control the delivery of blood and oxygen to tissues are unable to compensate for inadequate tissue delivery. Most data on secondary brain injury are derived from the ischemic stroke and traumatic brain injury (TBI) literature but are likely applicable to any neurologic insult in which cerebral autoregulation is impaired such as intracranial hemorrhage, subarachnoid hemorrhage, and conditions of elevated intracranial pressure (ICP).