A 26 year-old female college graduate student with no significant past medical history was struck by a motor vehicle while running and allegedly “flung 40 feet.” Primary trauma survey demonstrated a comminuted fracture of the left scapula and a non-comminuted fracture of the right inferior pubic rami as well as a left fronto-temporal intra-parenchymal hemorrhage (IPH), SAH, and a left cerebral convexity SDH (Fig. 10.2). A brain tissue oxygen monitor was placed after getting a single dose of mannitol for elevated intracranial pressure (ICP). Off sedation, the patient’s ICP increased to the 40 mmHg, and hypertonic saline was administered. ICP decreased to 20–25 mmHg with preservation of cerebral perfusion pressure (CPP). Intracranial pressure remained elevated despite maximal medical therapy and brain tissue oxygen (PbtO₂) values were below target. The patient was taken to the operating room (OR) emergently for a decompressive hemicraniectomy; PbtO₂ values improved after surgery. On post-injury day #2, the PbtO₂ fell to 10 mmHg; cerebral perfusion was augmented with induced hypertension and intravenous fluids. By post-injury day# 6 she was following commands and the brain tissue oxygen monitor was removed. She was extubated successfully the following day. On post-injury day #13 she was discharged to an acute brain injury rehab. She presented for an autologous cranioplasty 11 weeks post-injury and was noted to be weight bearing in therapy. Six-months post-injury she completed a 5 K race, returned to school and resumed working part-time. One year after her injury she ran a half-marathon.

Published guidelines and best practice statements have attempted to standardize the treatment and management of TBI [2, 3, 6]. The Brain Trauma Foundation (BTF) has developed evidence-based guidelines for both pre-hospital and in-hospital management of patients suffering from TBI. The BTF also created guidelines for special populations including children, soldiers and for those with concussion. The American College of Surgeons also recently published a Best Practice Statement for the management of TBI [3].

The initial evaluation of the TBI patient is guided by the BTF and focuses on basic life support, cervical stabilization and appropriate triage. Triage is based on the Glasgow Coma Scale (GCS) (Table 10.1). The GCS provides a standardized classification to the neurological assessment. The GCS encompasses a score of three assessed components (eye, verbal, and motor) for each individual patient. The three individual component scores, as well as the sum total, should be tallied and reported for use. If a sub-component cannot be tested due to intubation, sedation, or other factor, the reason should be noted. Severe TBI is defined as a GCS of 3–8, moderate TBI as a GCS of 9–12, and mild TBI by a GCS of 13–15 [1]. Although the GCS was established to triage patients in the trauma bay, serial assessments of the GCS may be useful to trend changes in exam and document response to interventions.

Patients with a GCS of ≤13 should be transported to the highest level trauma centre in the region for assessment and possible intervention by a neurosurgeon. Patients with a GCS of ≤15 and moderate severe extra-cranial injuries and Abbreviated Injury Score (AIS) (Table 10.2) of ≥3 should also be transferred to the highest level trauma centre in that region for assessment and possible intervention by a neurosurgeon and a multidisciplinary team [3].

The patient, bystanders, and/or emergency medical personnel typically provide the history leading to the diagnosis of TBI. Initial assessment should include documentation of abrasions, lacerations, soft tissue swelling of the head, presence of entrance and exit wounds, retro-auricular ecchymosis (Battle’s sign), periorbital ecchymosis (racoon’s eyes), hemotympanum, and CSF otorrhea or rhinorrhoea [2]. If no history is available, providers typically use clinical assessment and radiographic findings to determine the TBI diagnosis.

Initial treatment in the emergency department is guided by Advanced Trauma Life Support (ATLS) recommendations. Treatment includes monitoring of systemic oxygenation and blood pressure and targeting therapeutic thresholds (Table 10.3) [3]. Neurological assessment should be performed serially and neuroimaging should be obtained to guide operative intervention. Clinical signs of intracranial hypertension (e.g. Cushing response or pupillary dilation) should prompt empiric treatment and consideration of an ICP monitor. Laboratory assessments including blood alcohol level and urine toxicology screen should be performed and any coagulation derangement should be rapidly corrected, when appropriate.