Residency · Residency · Neurosurgery
Initial Assessment and Management of Severe Traumatic Brain Injury
Introduction
Severe traumatic brain injury is defined by a Glasgow Coma Scale score of 3 to 8 after resuscitation. TBI remains a leading cause of death and disability worldwide, particularly in young adults. The primary injury occurs at the moment of impact and is irreversible, but secondary brain injury from hypotension, hypoxia, and intracranial hypertension is potentially preventable and represents the primary target of acute management.
Primary and Secondary Survey
Prehospital Care
Airway management with early endotracheal intubation is required for patients with GCS of 8 or below or inability to protect the airway. Breathing management targets an oxygen saturation above 90 percent at all times while avoiding hyperventilation, with a target PaCO2 of 35 to 40 mmHg. Circulation management prevents hypotension, defined as systolic blood pressure below 90 mmHg, through aggressive fluid resuscitation with isotonic crystalloid. Disability assessment includes GCS scoring, pupillary examination, and identification of lateralizing signs. A single episode of hypotension with systolic blood pressure below 90 doubles mortality in severe TBI.
Emergency Department Assessment
Assessment follows ATLS protocol with primary survey, resuscitation, and secondary survey. GCS is reassessed after adequate resuscitation and before administration of sedation or paralytics. Pupillary examination identifies a unilateral fixed dilated pupil suggesting ipsilateral uncal herniation. Associated injuries are identified, including cervical spine injury which is present in 5 to 10 percent of severe TBI patients, along with thoracic and abdominal trauma. Blood alcohol and toxicology screening are obtained.
Imaging
Non-contrast CT of the head is performed immediately for all severe TBI, identifying mass lesions requiring surgery. Key findings include epidural hematoma, acute subdural hematoma, contusions, traumatic subarachnoid hemorrhage, diffuse axonal injury, and pneumocephalus. CT of the cervical spine is mandatory in all severe TBI patients. CT angiography is considered for skull base fractures, penetrating injury, or concern for vascular injury. The Marshall CT classification or Rotterdam CT score provides prognostication.
Initial Medical Management
Airway and Ventilation
Rapid sequence intubation is performed with cervical spine immobilization maintained. Succinylcholine is avoided if hyperkalemia is a concern, with rocuronium preferred. Ventilator settings target a PaO2 above 60 mmHg and PaCO2 of 35 to 40 mmHg. Prophylactic hyperventilation is avoided because it causes cerebral vasoconstriction and reduces cerebral blood flow, potentially worsening ischemia.
Hemodynamic Targets
Systolic blood pressure is maintained at or above 100 mmHg per Brain Trauma Foundation fourth edition guidelines for patients aged 50 to 69 years, and at or above 110 mmHg for patients aged 15 to 49 years. Vasopressors, primarily norepinephrine, are used when fluid resuscitation is insufficient. Hypotonic fluids such as D5W and 0.45 percent saline are avoided because they worsen cerebral edema.
ICP-Directed Therapy
An ICP monitor, either intraparenchymal or external ventricular drain, is inserted for patients with GCS 3 to 8 and an abnormal CT scan. The target is ICP below 22 mmHg and cerebral perfusion pressure of 60 to 70 mmHg. An EVD provides the additional advantage of therapeutic CSF drainage. Treatment escalation follows a stepwise approach: head of bed elevation to 30 degrees, sedation and analgesia, osmotherapy, and CSF drainage.
Seizure Prophylaxis
Phenytoin or levetiracetam is administered for 7 days to prevent early post-traumatic seizures. No benefit has been demonstrated for late seizure prophylaxis beyond 7 days. Continuous EEG monitoring is recommended for patients with unexplained decreased consciousness to detect subclinical seizures.
Temperature Management
Normothermia at 36 to 37 degrees Celsius is maintained, and fever is aggressively treated. Therapeutic hypothermia has not shown consistent benefit in randomized controlled trials, including the Eurotherm and POLAR trials.
Surgical Indications
Epidural hematoma warrants surgery when thickness exceeds 15 millimeters, midline shift exceeds 5 millimeters, or neurological deterioration occurs. Acute subdural hematoma requires surgery when thickness exceeds 10 millimeters, midline shift exceeds 5 millimeters, or GCS drops by 2 or more points. Depressed skull fractures are repaired when they are open, depressed greater than the skull thickness, or involve a dural breach. Posterior fossa hematomas require early surgical evacuation due to the risk of rapid brainstem compression from the limited space. Decompressive craniectomy is considered for refractory intracranial hypertension.
Coagulopathy Management
Trauma-induced coagulopathy occurs in 20 to 30 percent of severe TBI patients. Coagulation studies, platelet count, and fibrinogen are checked on arrival. Anticoagulants are reversed with vitamin K, fresh frozen plasma, or prothrombin complex concentrate for warfarin, and idarucizumab for dabigatran. Tranexamic acid administered within 3 hours of injury showed modest benefit in the CRASH-3 trial for mild-to-moderate TBI.
Clinical Pearls
Prevention of secondary brain injury through avoidance of hypotension with systolic blood pressure below 90 and hypoxia with oxygen saturation below 90 percent is the single most impactful intervention in early TBI management. The GCS motor score is the most predictive individual component for outcome and should be carefully documented before sedation is administered. A lucid interval followed by rapid deterioration is the classic presentation for epidural hematoma and constitutes a neurosurgical emergency requiring immediate surgical evacuation. Early neurosurgical consultation and transfer to a Level I trauma center are associated with improved outcomes in severe TBI.
References
- Carney N, Totten AM, O'Reilly C, et al. Guidelines for the management of severe traumatic brain injury, Fourth Edition. Neurosurgery. 2017;80(1):6-15.
- CRASH-3 trial collaborators. Effects of tranexamic acid on death, disability, vascular occlusive events and other morbidities in patients with acute traumatic brain injury. Lancet. 2019;394(10210):1713-1723.
- Stocchetti N, Maas AIR. Traumatic intracranial hypertension. N Engl J Med. 2014;370(22):2121-2130.
- Bullock MR, Chesnut R, Ghajar J, et al. Surgical management of acute subdural hematomas. Neurosurgery. 2006;58(3 Suppl):S16-24.