Identification of severe traumatic brain injury requires two criteria to be met. First, the Glasgow Coma Score (GCS) must
be 8 or less. The GCS was first described in 1974 by Graham Teasdale and Bryan J. Jennett, professors of neurosurgery at the University of Glasgow, Scotland. In 1981, they approached F.A. Davis, the author of a textbook Management of Head Injuries who included the scoring system for identification of different levels of TBI.

The next criteria for a severe TBI is an abnormal brain computed tomography (CT) with findings such as contusion, hematoma, diffuse axonal injury (DAI), compressed basal cistern, subarachnoid hemorrhage (SAH), and/or other clear signs of brain injury. When only an abnormal GCS is present, it is possible to be due to something other than TBI. When an injured patient arrives in an emergency department (ED), these two assessments are done to identify a severe TBI patient. When these criteria are met, the patient should be moved to a Neurotrauma ICU, a part of the recognized Trauma Center, as soon as possible, provided other types of operative treatment are not more urgently needed. Placement of an intracranial pressure monitor should be considered in the multiple-injured TBI patient, simultaneously with the non-neurosurgical operative procedures.

We recommend intracranial pressure (ICP) monitors for assessing the moment-to-moment status of your patient. Generally, a ventriculostomy type monitor is superior to an intraparenchymal (Bolt) monitor. The ventriculostomy can accurately determine the intracranial pressure but also allows the neurophysicians to drain cerebrospinal fluid (CSF). The latest recommendation for ICP monitors is to have an electronic continuous record with instantaneous alerts for significant increases to allow immediate interventions per protocol. Many devices are available for measuring brain oxygen levels as well as oxygen from the jugular bulb. The value of these measurements is yet to be determined by the BTF and AANS [14,15,16,17,18,19].

An understanding of the Monro-Kellie doctrine is essential. In 1783, Alexander Monro deduced that the cranium was a “rigid box” filled with a “nearly incompressible brain” and that its total volume tends to remain constant. The doctrine states that any increase in the volume of the cranial contents (e.g., brain, blood, or cerebrospinal fluid), will elevate intracranial pressure. Furthermore, if one of these three elements increases in volume, it must occur at the expense of the volume of the other two elements. In 1824, George Kellie confirmed many of Monro’s early observations. If as a result of trauma a hematoma forms on the outside of the brain (epidural hematoma), under the dura (subdural hematoma), or within the brain itself, the space occupied by the hematoma must result in a commensurate decrease of the intracranial blood or CSF volume. Once these compensatory mechanisms are exhausted, intracranial pressure will rise rapidly, and brain herniation may occur. Cerebral edema can mimic an expanding mass lesion, with similar pathophysiology, and potential for the irreversible damage associated with uncal and/or tonsillar herniation (see graph in Fig. 162.1).

In general, the reaction to an intracranial mass or cerebral edema is to reduce the amount of venous blood and CSF within the skull. The body’s response to the injury is to keep the pressure inside the skull as close to normal as possible by reducing those volumes that can be reduced. When a sudden increase of ICP occurs and the patient has a ventriculostomy, the neurointensivist may drain additional CSF from this closed box. This in turn helps to keep the ICP under control while other measures are taken to reduce the ICP in a more lasting fashion. We will discuss more about this under patient management.

The next consideration for the severe TBI patient is determining what other injuries the patient might have. A qualified trauma surgeon must be involved to assist the neurointensivist with the fluid/blood product management. For example, a patient with a class III anterior posterior pelvic fracture will lose huge amounts of blood even if managed by a trauma orthopedist with pelvic circumference reduction. This is an indication for a pulmonary artery catheter (PAC) (or one of the newer devices for monitoring pressures and cardiac output) to monitor the resuscitation as closely as possible. The goal is maintaining the patient’s systolic pressure at or above 90 torr. In the book, Management and Prognosis of Severe Traumatic Brain Injury, a joint project of the Brain Trauma Foundation and American Association of Neurological Surgeons, class two evidence states that allowing the systolic BP to drop below 90 torr will likely produce secondary brain injury. The BTF class two evidence criteria are clinical studies in which the data was collected prospectively or retrospective analyses that were based on clearly reliable data. Types of studies so classified include: observational studies, cohort studies, prevalence studies, and case control studies. Class two evidence shows that post injury hypotension has dramatic impact on the brain injury outcome. We recommend using the PAC data to assist in fluid/blood product management to maintain a PCWP between 10 to 15 mm Hg and a CI of 2.6 L per minute per m². Invasive hemodynamic monitoring may also help avoid fluid overload and possibly associated increases in cerebral edema. A new monitoring device is now being evaluated for these multiply-injured patients. The use of The InSpectra™, StO₂ Tissue Oxygenation Monitor will provide continuous, real-time information for perfusion status monitoring and a new hemodynamic parameter (StO₂) to assist clinicians in the early detection of inadequate tissue perfusion (hypoperfusion). This device would noninvasively monitor hemodynamic status and tissue oxygenation, both of which are critical for severe TBI patients [19].