11. Traumatic Brain Injury

Quick Recap

Neurology System, Protocol 11/12. Builds on the Raised ICP protocol's tiered algorithm with TBI-specific evidence, CPP management, and concurrent spine injury considerations.

1. Epidemiology

Severe head trauma is a leading cause of morbidity/mortality worldwide, especially in young adults. ~2.5 million Americans treated for TBI annually; ~70,000 US deaths/year. Mortality in severe TBI has decreased from ~50% to ~25% over three decades — largely attributed to improved recognition and treatment of SECONDARY brain injury (occurring hours-days after the initial trauma), not the primary impact itself, which is already done by the time the patient reaches care.

2. Classification

By GCS (Glasgow Coma Scale — eye/verbal/motor components, 3-15 total):

By morphology: skull fractures (vault — linear vs stellate/compound, depressed vs non-depressed; basilar — with/without CSF leak or cranial nerve palsy); intracranial lesions (focal — epidural hematoma, subdural hematoma, intracerebral hemorrhage; diffuse — hypoxic/ischemic injury, diffuse axonal injury, multiple contusion, concussion).

GCS <=13 with moderate-severe extracranial injuries warrants rapid transfer to a higher level of care.

3. Immediate Stabilization (ABCDE) — Primary Survey

Airway takes precedence even with obvious head injury (do not let visible head trauma distract from ABC sequence):

• Secure cervical spine with a collar — unstable C-spine injury occurs in 5-6% of TBI cases; risk factors: MVC, assault, falls, GCS <8
• RSI with in-line cervical immobilization (collar off during the actual intubation attempt to avoid worsening injury, reapplied immediately after, pending radiologic clearance)
• Prevent hypoxemia: avoid PaO2 <60 mmHg or SpO2 <90%
• RSI drug choices: succinylcholine or rocuronium as paralytic — succinylcholine's small ICP rise is not clinically significant and should not deter its use when otherwise indicated; fentanyl 1mcg/kg as an opiate adjunct; no evidence supports lidocaine use during intubation for this indication despite historical teaching (contrast with the ICH protocol's lidocaine-pretreatment recommendation — evidence quality/consistency differs across these related but distinct populations)
• Sedative choice: propofol and thiopental most commonly used (both can cause hypotension); etomidate offers cardiovascular stability but carries adrenal suppression risk — no single agent is clearly superior; choice is individualized to hemodynamic status

Breathing: avoid both hypoxemia and hyperventilation as routine strategy (see Raised ICP protocol — hyperventilation reserved for acute herniation bridging only).

Circulation — fluid choice and CPP:

• Fluid resuscitation, blood transfusion, and/or vasopressors as needed for ongoing bleeding/hypotension
• Saline is PREFERRED over albumin for resuscitation — albumin has been shown to INCREASE mortality in TBI patients (a specific, important exception to general critical care fluid practice) — colloids in general offer no additional benefit over crystalloid in this population
• Keep SBP >100-110 mmHg until a CPP value can be directly measured
• Once ICP monitor placed: CPP goal 60-70 mmHg (CPP = MAP − ICP); use vasopressors to augment MAP/CPP in refractory cases, but avoid aggressive attempts to push CPP above 70 mmHg with fluids/pressors — this ceiling matters as much as the floor, given evidence that over-augmentation offers no benefit and carries its own risk (e.g., ARDS from aggressive fluid/pressor use)
• Labetalol is the drug of choice for hypertensive emergency control in TBI specifically

~15% of TBI patients have an associated spinal cord injury — stabilize/immobilize the spine as an initial priority alongside head injury management (see also Section 8 for concurrent spinal injury management specifics).

Checklist:

4. Imaging

CT head in ALL moderate-severe TBI. Mild TBI CT indications: open/depressed skull fracture, signs of basilar skull fracture, >2 vomiting episodes, age >65, anticoagulant use, seizure — apply these to decide which "mild" (GCS 13-15) patients still need imaging rather than scanning universally.

5. ICP Monitoring — TBI-Specific Indications

Indicated for: GCS 3-8 (all severe TBI); ALSO indicated in severe TBI with a NORMAL CT scan if: age >40, unilateral or bilateral motor posturing, or SBP <90 mmHg — an important point that a normal initial CT does NOT rule out the need for monitoring in high-risk patients.

Management based on ICP monitoring reduces in-hospital and 2-week post-injury mortality — among the strongest evidence bases for ICP-monitor-driven management across any etiology in this system (see Raised ICP protocol Section 5).

Treatment threshold: ICP >20-22 mmHg (sources vary slightly; treat consistently and sustained elevation, not isolated spikes).

In ~half of TBI deaths, elevated ICP with herniation is the primary cause of death — underscoring why aggressive, monitored management matters.

6. ICP/CPP Management — Follows the Raised ICP Protocol's Tiered Algorithm

Apply the full tiered algorithm from the Raised ICP protocol (universal measures -> first-tier osmotherapy/CSF drainage -> second-tier barbiturate coma/hypothermia -> third-tier decompressive craniectomy), with TBI-specific emphasis:

• Universal measures: HOB 30 degrees, chin midline (avoid jugular compression), normocarbia, normothermia, euvolemia, avoid hyponatremia
• Seizure prophylaxis IS recommended for TBI patients at high risk (phenytoin 20mg/kg load, then 5-8mg/kg/day) — this is a notable EXCEPTION to the no-prophylaxis rule established for Stroke and ICH in this system; TBI's structural cortical injury and hemorrhage burden carries a different early post-traumatic seizure risk profile that has supported prophylaxis in evidence to date, though this should be time-limited (typically 7 days) rather than indefinite
• Glucose control 80-140 mg/dL
• Early enteral nutrition within 72h

7. Prognosis

GCS <8 carries ~30% mortality risk as a general rule. Vegetative or minimally conscious state carries a poor chance of meaningful recovery. However, functional independence or partial independence can occur in >50% of severe TBI survivors over a period of YEARS if initial aggressive management is pursued — this matters directly for early goals-of-care conversations: early severity does not necessarily predict long-term trajectory, and premature therapeutic nihilism based on initial presentation alone is not well supported.

Poor-outcome risk factors: low GCS (especially motor component specifically), increasing age, bilaterally absent pupillary light reflex, associated injuries, abnormal CT, hypotension, hypoxemia, elevated ICP, reduced CPP, bleeding diathesis, fever.

CT findings associated with poor prognosis: absent/compressed basal cisterns, traumatic SAH, midline shift degree, any abnormality on initial CT.

Outcome measurement tools: Functional Independence Measure (FIM), Glasgow Outcome Scale (GOS), Disability Rating Scale (DRS) — useful for tracking recovery trajectory and rehabilitation planning over the (potentially years-long) recovery window.

8. Concurrent Traumatic Spine Injury (Frequently Co-occurring)

~5% of TBI patients have an associated spinal injury; conversely, ~25% of spinal injury patients have at least mild TBI plus limb/visceral injury — actively screen for both directions of this association, not just TBI-to-spine.

Distribution: ~55% cervical (quadriparesis risk), 15% thoracic, 15% thoracolumbar junction, 15% lumbosacral. Up to 10% of cervical spine fractures have a SECOND, non-contiguous vertebral fracture — image the entire spine, mirroring the same "don't just image the symptomatic level" principle established for malignant spinal cord compression in the Brain Tumors protocol.

Management:

• Full ATLS assessment avoiding hypotension, bradycardia, hypoxia
• Early intubation/ventilation recommended for high cervical injuries (C1-C5) given diaphragmatic involvement risk
• Cervical spine immobilization until an unstable fracture is definitively ruled out
• Complete spinal imaging (X-ray or CT) for any suspected cervical spine injury
• Urgent neurosurgical consultation
• MAP augmentation with norepinephrine for at least the first 72 hours (up to 7 days) post-injury, goal MAP >=85 mmHg for blunt/incomplete penetrating spinal cord injury — this specific, sustained MAP target for spinal cord perfusion is distinct from (and should not be confused with) the CPP target used for the brain injury itself

9. Long-Term Complications to Anticipate (Relevant to Prolonged ICU/Rehabilitation Course)

ARDS/negative pressure pulmonary edema, paroxysmal sympathetic hyperactivity/stress cardiomyopathy, hypothalamic-pituitary-adrenal dysfunction/SIADH/cerebral salt wasting/diabetes insipidus, hydrocephalus, heterotopic ossification, spasticity, chronic traumatic encephalopathy/post-traumatic headache and depression/cognitive impairment, GI/GU complications, gastric ulceration and DVT — anticipate and screen for this list proactively rather than reactively, particularly in patients with a prolonged ICU/rehabilitation course.

10. Organ Support

Mechanical ventilation with ICP-conscious strategy; ICP/CPP-directed therapy per Sections 5-6; saline-based (not albumin) fluid resuscitation; vasopressors for CPP/spinal cord perfusion augmentation as indicated; standard ICU supportive care with proactive screening for the long-term complications in Section 9.

11. Consultation Matrix

12. Monitoring Framework

Continuous ICP/CPP monitoring, serial GCS/neuro exam, temperature (active normothermia), glucose control, screening for the long-term complication list (Section 9) as the ICU course extends, seizure monitoring during the prophylaxis window.

13. Complications

Secondary brain injury (hypoxia, hypotension, elevated ICP, seizures — the primary preventable mortality drivers), herniation, the extensive long-term complication list in Section 9, concurrent spinal cord injury complications if present. Prevention: aggressive secondary injury prevention (the single biggest lever for the 3-decade mortality improvement), saline-based resuscitation, appropriate CPP targeting without over-augmentation, time-limited seizure prophylaxis. Rescue: full Raised ICP tiered algorithm, decompressive craniectomy, spinal cord perfusion pressure augmentation for concurrent spine injury.

14. Escalation & De-escalation

Escalate: ICP refractory to first-tier measures -> second-tier (barbiturate coma/hypothermia) -> third-tier (decompressive craniectomy) per Raised ICP protocol algorithm.

De-escalate: ICP stable/controlled, neuro exam stable or improving -> wean ICP-directed therapy, discontinue seizure prophylaxis at the appropriate time-limited endpoint, transition to rehabilitation-focused care given the years-long recovery potential.

15. ICU Discharge Criteria

ICP stable off aggressive tiered therapy, hemodynamically stable, seizure prophylaxis window completed or ongoing outpatient plan established, concurrent spinal injury stabilized/managed, rehabilitation plan and outcome measure baseline (FIM/GOS/DRS) documented.

16. Documentation & Medicolegal Checklist

17. Key Guidelines

Carney N, Totten AM, O'Reilly C, et al. Guidelines for the management of severe traumatic brain injury, 4th ed. Neurosurgery. 2017;80(1):6-15 (Brain Trauma Foundation) — primary evidence base.

18. Landmark Trials

Hutchinson PJ, Kolias AG, Timofeev IS, et al. Trial of decompressive craniectomy for traumatic intracranial hypertension (RESCUEicp). N Engl J Med. 2016;375:1119-1130 — see Raised ICP protocol for the disability-vs-mortality tradeoff this trial revealed. SAFE study investigators — albumin vs saline in critically ill patients, TBI subgroup analysis showing increased mortality with albumin, underpinning the saline-preference recommendation.

19. Controversies

Seizure prophylaxis duration and threshold in TBI (unlike the clearer no-prophylaxis stance in Stroke/ICH) remains an area of ongoing practice variation — most protocols limit to ~7 days, but the exact risk-benefit threshold for extending or omitting prophylaxis in specific injury patterns is not fully settled. Optimal CPP target range (60-70 vs individualized autoregulation-guided targets via multimodal monitoring) is an active research area — fixed-threshold CPP management may not be optimal for all patients given individual variation in cerebral autoregulation status. The precise ICP treatment threshold (20 vs 22 mmHg) varies slightly across sources without full consensus.

20. References

1. Traumatic Brain Injury and Elevated Intracranial Pressure chapter. Washington Manual of Critical Care, 4th ed, 2025 (Ch. 63).
2. Zirpe K, Nimavat B. Traumatic Brain and Spinal Injury. ICU Protocols: A Step-wise Approach, 2nd ed. Springer; 2020 (Ch. 11).
3. Carney N, Totten AM, O'Reilly C, et al. Guidelines for the management of severe traumatic brain injury, 4th ed. Neurosurgery. 2017;80(1):6-15.
4. SAFE Study Investigators. Saline or albumin for fluid resuscitation in patients with traumatic brain injury. N Engl J Med. 2007;357(9):874-884.
5. Hutchinson PJ, Kolias AG, Timofeev IS, et al. Trial of decompressive craniectomy for traumatic intracranial hypertension. N Engl J Med. 2016;375:1119-1130.

See also: Raised ICP (Neurology System) for the full tiered ICP management algorithm this protocol builds upon.