Traumatic Brain Injury Management
Initial Assessment and Severity Classification
Severe TBI patients must be managed by a prehospital medicalized team and transferred immediately to a specialized neurosurgical center, as this approach significantly reduces mortality and improves neurological outcomes. 1
- Classify severity using Glasgow Coma Scale (GCS): severe (GCS ≤8), moderate (GCS 9-13), mild (GCS 14-15), with the motor component being most reliable in sedated patients 2
- Assess pupil size and reactivity repeatedly during initial phase, as these are critical prognostic factors 2
- Perform brain and cervical CT scan without delay in all severe and moderate TBI patients 1, 2
Hemodynamic Management - Critical Priority
Maintain systolic blood pressure >110 mmHg at all times, as even a single episode of hypotension below this threshold markedly increases mortality. 1, 3
- A single episode of systolic blood pressure <90 mmHg during early TBI phase significantly worsens neurological outcome 1
- Use vasopressors immediately if hypotension develops rather than waiting for fluid resuscitation 3
- Avoid hypotensive sedative agents during induction and maintenance of sedation 1, 3
- Maintain mean arterial pressure ≥80 mmHg in severe TBI 2
- The combination of hypotension and hypoxemia (SaO₂ <90%) carries a 75% mortality rate 2
Airway and Ventilation Control
- Intubate early if GCS is compromised or risk of deterioration exists 3
- Maintain end-tidal CO₂ between 30-35 mmHg prior to obtaining arterial blood gas samples 1
- Monitor end-tidal CO₂ continuously to prevent both hypercapnia and hypocapnia 3
- Adjust mechanical ventilation to facilitate central venous return 3
Imaging Strategy
Perform brain and cervical CT with bone windows immediately upon arrival to identify primary lesions and guide neurosurgical intervention. 1, 2
- Use double fenestration (central nervous system and bone windows) to fully characterize injuries 1, 3
- Obtain CT angiography of supra-aortic and intracranial vessels early in patients with risk factors for traumatic arterial dissection 1, 3
- Basilar skull fractures are a specific high-risk factor requiring CT angiography 3
- Repeat CT at 6-12 hours if initial scan shows associated intracranial injury 3
Neurosurgical Consultation and Intervention
Immediate neurosurgical evaluation is required for acute subdural/epidural hematoma, multiple hemorrhagic contusions, significant mass effect or midline shift, or deteriorating neurological examination. 3
Early phase neurosurgical indications include: 2
- Evacuation of symptomatic extradural hematoma
- Evacuation of significant acute subdural hematoma
- Drainage of acute hydrocephalus
- Closure of displaced open skull fracture
Intracranial Pressure Management
For persistent intracranial hypertension despite sedation and correction of secondary insults: 2
- Perform external ventricular drainage as first-line intervention
- Use osmotic diuretics (mannitol) to reduce intracranial pressure
- Administer hypertonic saline for clinical transtentorial herniation
- Consider decompressive craniectomy for refractory intracranial hypertension after multidisciplinary discussion
Monitoring and Admission
- Admit all patients with basilar skull fractures for close neurological observation with serial examinations, even if GCS is 15 3
- Monitor for delayed complications including vascular injury/dissection 3
- Transcranial Doppler can assess brain perfusion; concerning findings include diastolic flow velocity <20 cm/s and pulsatility index >1.4 1, 2
Critical Pitfalls to Avoid
- Do NOT use corticosteroids for TBI management, as they provide no benefit on mortality or neurological outcomes 2
- Do NOT use biomarkers in clinical routine to assess initial severity, as uncertainties remain regarding normal ranges and clinical utility 1
- Do NOT discharge patients with basilar skull fractures without adequate observation, even with GCS 15 3
- Do NOT miss associated vascular injuries—always obtain CT angiography in high-risk fracture patterns 3
- Do NOT allow any episode of arterial hypotension; prevention is critical through continuous sedation rather than boluses and immediate correction of hypovolemia 1