Traumatic Brain Injury — Part 2: Initial Management & Resuscitation
Airway management and RSI in TBI, oxygenation and ventilation targets, blood pressure management, seizure prophylaxis, coagulopathy reversal, TXA (CRASH-3), and cerebral herniation emergency management.
1. Airway Management in TBI
1.1 Indications for Endotracheal Intubation
Definitive airway management with endotracheal intubation is one of the most critical early interventions in TBI. Indications include.1 2
| Indication | Rationale |
|---|---|
| GCS ≤ 8 | Inability to protect airway; universal threshold for intubation in severe TBI |
| Declining GCS (drop of ≥ 2 points) | Indicates clinical deterioration and impending airway compromise |
| Loss of protective airway reflexes | Aspiration risk |
| Hypoxemia refractory to supplemental oxygen | PaO2 < 60 mmHg or SpO2 < 90% |
| Hypercarbia (PaCO2 > 45 mmHg) | Increased ICP from cerebral vasodilation |
| Combative patient requiring sedation for imaging/transport | Safety and diagnostic necessity |
| Bilateral mandibular fractures or massive facial trauma | Structural airway compromise |
| Anticipated clinical course (prolonged transport, need for emergent surgery) | Proactive airway management |
Critical Warning: Avoid nasal intubation in patients with suspected basilar skull fracture (raccoon eyes, Battle sign, CSF rhinorrhea/otorrhea, hemotympanum) due to the risk of intracranial tube passage through a disrupted cribriform plate. Oral intubation with in-line cervical spine stabilization is the preferred route.2
1.2 Rapid Sequence Intubation (RSI) in TBI
RSI is the method of choice for emergency intubation in TBI patients. The goals are to achieve rapid, controlled intubation while minimizing ICP elevations and maintaining cerebral perfusion pressure.3
Pre-Intubation Preparation
| Step | Action |
|---|---|
| Preoxygenation | 100% O2 via NRB mask or BVM with PEEP valve for ≥ 3 minutes (or 8 vital capacity breaths). Target SpO2 ≥ 95% before attempt |
| Position | Head of bed elevated 20–30° if no spinal precautions; in-line cervical stabilization (remove anterior collar, maintain manual stabilization) |
| Equipment | Prepare two laryngoscopes (video preferred), bougie, surgical airway kit |
| Hemodynamic optimization | Ensure IV access; prepare push-dose vasopressor (phenylephrine 100 mcg/mL or epinephrine 10 mcg/mL) for post-intubation hypotension |
RSI Medications for TBI
| Phase | Medication | Dose | Notes |
|---|---|---|---|
| Pretreatment | Fentanyl | 1–3 mcg/kg IV over 30–60 sec | Blunts sympathetic response to laryngoscopy; optional; avoid in hypotension |
| Lidocaine | 1.5 mg/kg IV | Traditionally used to blunt ICP rise; evidence for benefit is weak; optional | |
| Induction | Ketamine | 1–2 mg/kg IV | Now preferred in TBI. Previously avoided due to theoretical ICP concerns, but multiple studies demonstrate hemodynamic stability without clinically significant ICP elevation. Neuroprotective NMDA antagonism. Ideal for hemodynamically unstable patients.4 |
| Etomidate | 0.3 mg/kg IV | Hemodynamically neutral. Risk of adrenal suppression with single dose is debated. Does not lower ICP | |
| Propofol | 1–2 mg/kg IV | Lowers ICP but causes significant hypotension — avoid in hypotensive patients | |
| Midazolam | 0.1–0.3 mg/kg IV | Slower onset; less predictable; generally not first-line for RSI | |
| Paralytic | Succinylcholine | 1.5 mg/kg IV | Onset 45–60 sec; duration 6–10 min. Theoretical ICP rise from fasciculations is clinically insignificant. Avoid if hyperkalemia risk (delayed presentation > 72h with denervation injury) |
| Rocuronium | 1.2 mg/kg IV | Onset 45–60 sec; duration 45–70 min. Preferred by many due to absence of hyperkalemia risk and can be reversed with sugammadex (16 mg/kg) |
Key Evidence on Ketamine in TBI: A systematic review and meta-analysis demonstrated that ketamine does not increase ICP and may actually reduce ICP in mechanically ventilated patients with TBI. Multiple trauma society guidelines now list ketamine as an acceptable induction agent for TBI, including for prehospital RSI.4
1.3 Post-Intubation Management
| Parameter | Target | Rationale |
|---|---|---|
| SpO2 | ≥ 94% | Avoid hypoxemia (associated with doubled mortality in severe TBI) |
| PaCO2 | 35–40 mmHg (normocapnia) | Hyperventilation causes cerebral vasoconstriction → ischemia; only use brief hyperventilation as a bridge for herniation |
| ETCO2 | 35–40 mmHg | Correlate with ABG early; ETCO2 may underestimate PaCO2 by 3–8 mmHg |
| Head position | HOB 30°, midline | Promotes venous drainage; avoid neck flexion, tight cervical collars, and internal jugular central lines on the ipsilateral side |
| Sedation | Propofol or midazolam + fentanyl | Prevent coughing/bucking on ETT which raises ICP |
2. Oxygenation and Ventilation
2.1 Oxygenation Targets
Both hypoxemia and extreme hyperoxia are harmful after TBI.5
| Parameter | Target | Evidence Level |
|---|---|---|
| SpO2 | ≥ 90% (preferably ≥ 94%) | Level III recommendation. Even a single episode of SpO2 < 90% is associated with significantly worse outcomes |
| PaO2 | ≥ 60 mmHg (preferably 80–120 mmHg) | Level III recommendation |
| Avoid extreme hyperoxia | PaO2 > 300 mmHg may worsen oxidative stress | Emerging evidence; aim for normoxia once stabilized |
2.2 Ventilation Targets
| Parameter | Target | Rationale |
|---|---|---|
| PaCO2 | 35–40 mmHg (normocapnia) | Hyperventilation (PaCO2 < 35) causes cerebral vasoconstriction, reduces cerebral blood flow, and may cause ischemia |
| Tidal volume | 6–8 mL/kg IBW | Lung-protective ventilation; TBI patients at high risk for ARDS |
| PEEP | 5–8 cmH2O (up to 12 if needed for oxygenation) | PEEP > 15 may impair cerebral venous drainage; monitor ICP if high PEEP required |
| Respiratory rate | Adjust to achieve target PaCO2 | Typically 14–18 breaths/min |
Critical Warning — Prophylactic Hyperventilation: Prolonged prophylactic hyperventilation (PaCO2 ≤ 25 mmHg) is contraindicated in the first 24 hours after severe TBI and should be avoided throughout the acute phase. This is a Level IIB recommendation from the fourth edition of the severe TBI management guidelines. Brief, controlled hyperventilation (PaCO2 30–35 mmHg) is reserved ONLY as a temporizing measure for acute herniation.5
3. Blood Pressure Management and Cerebral Perfusion
3.1 Avoiding Hypotension — The Single Most Important Systemic Factor
Hypotension (SBP < 90 mmHg) is the most powerful modifiable predictor of poor outcome in TBI. A single episode of hypotension doubles mortality in severe TBI.5 6
| Recommendation | Target | Evidence Level |
|---|---|---|
| Avoid SBP < 90 mmHg | Minimum SBP ≥ 90 mmHg at all times | Level III |
| SBP ≥ 100 mmHg for patients age 50–69 | Optimal threshold based on IMPACT/BTF analysis | Level III |
| SBP ≥ 110 mmHg for patients age 15–49 or > 70 | Higher threshold may improve outcomes | Level III |
| MAP target | ≥ 80 mmHg (to maintain CPP 60–70 once ICP monitored) | Level II |
3.2 Cerebral Autoregulation
In the uninjured brain, cerebral blood flow (CBF) remains constant across a MAP range of approximately 50–150 mmHg through autoregulatory mechanisms. In TBI, autoregulation is frequently impaired, making CBF directly pressure-dependent. This means.6
- Hypotension → direct reduction in CBF → cerebral ischemia → secondary injury
- Hypertension → may worsen cerebral edema and hemorrhage expansion in regions with disrupted blood-brain barrier
3.3 Fluid Resuscitation
| Recommendation | Detail |
|---|---|
| First-line fluid | Isotonic crystalloid (0.9% NaCl or lactated Ringer’s) |
| Avoid hypotonic fluids | D5W, 0.45% NaCl, and other hypotonic solutions worsen cerebral edema |
| Avoid albumin | The SAFE trial demonstrated increased mortality with albumin resuscitation in TBI patients (RR 1.63 at 24 months)7 |
| Blood products | Transfuse PRBCs for Hgb < 7 g/dL; consider higher threshold (< 10) in patients with brain tissue hypoxia |
| Vasopressors | Norepinephrine is the first-line vasopressor for TBI patients with hypotension refractory to volume resuscitation. Phenylephrine is an alternative. Avoid vasopressin as first-line (reduces CBF) |
SAFE Trial Evidence: The Saline vs. Albumin Fluid Evaluation (SAFE) study demonstrated that 4% albumin resuscitation in TBI patients was associated with significantly higher mortality compared to 0.9% saline (33.2% vs. 20.4%; RR 1.63; 95% CI 1.17–2.26). Albumin should NOT be used for resuscitation in TBI patients.7
4. Seizure Prophylaxis
4.1 Risk Factors for Post-Traumatic Seizures
Post-traumatic seizures (PTS) are classified by timing.8 9
| Classification | Timing | Clinical Significance |
|---|---|---|
| Immediate | < 24 hours | Early PTS; prophylaxis effective |
| Early | Within 7 days | Early PTS; prophylaxis effective |
| Late | > 7 days | Post-traumatic epilepsy; prophylaxis NOT effective for prevention |
Risk Factors for Early Post-Traumatic Seizures:
| Risk Factor |
|---|
| GCS ≤ 10 |
| Cortical contusion |
| Depressed skull fracture |
| Subdural hematoma |
| Epidural hematoma |
| Intracerebral hematoma |
| Penetrating brain injury |
| Seizure within 24 hours of injury |
| Chronic alcohol use |
4.2 Seizure Prophylaxis Recommendations
| Recommendation | Detail | Evidence |
|---|---|---|
| Prophylaxis indicated for | Severe TBI (GCS ≤ 8) to prevent early PTS (within 7 days) | Level IIA |
| Duration | 7 days from injury; do NOT continue beyond 7 days for prophylaxis alone | Level IIA — Prophylaxis does not prevent late PTS or post-traumatic epilepsy8 |
| Preferred agent | Levetiracetam (Keppra) 500–1000 mg IV/PO q12h (20 mg/kg load, then 500–1000 mg q12h) | Comparable efficacy to phenytoin with more favorable side effect profile; no need for drug level monitoring9 |
| Alternative agent | Phenytoin (Dilantin) 20 mg/kg IV loading dose (max rate 50 mg/min), then 100 mg IV/PO q8h | Level IIA; historically the standard. Requires drug level monitoring (target total 10–20 mcg/mL, free 1–2 mcg/mL). Risk of hypotension with rapid IV loading |
| NOT recommended | Valproic acid for seizure prophylaxis in severe TBI | Level III — Trend toward higher mortality in CRASH trial subgroup |
| Prophylaxis NOT indicated for | Mild TBI (GCS 14–15) with normal CT | Insufficient evidence of benefit |
4.3 Levetiracetam vs. Phenytoin
| Feature | Levetiracetam | Phenytoin |
|---|---|---|
| Efficacy for early PTS | Equivalent | Standard reference |
| Drug level monitoring | Not required | Required (narrow therapeutic index) |
| Drug interactions | Minimal | Extensive (CYP450 inducer) |
| Adverse effects | Somnolence, irritability | Hypotension (IV loading), cardiac arrhythmia, Stevens-Johnson syndrome, purple glove syndrome |
| Cost | Higher (though now generic) | Lower |
| Hepatotoxicity | Rare | Possible |
| IV-to-PO conversion | 1:1 | 1:1 (approximately) |
4.4 Treatment of Active Post-Traumatic Seizures
| Line | Agent | Dose |
|---|---|---|
| First-line | Lorazepam | 0.1 mg/kg IV (max 4 mg per dose, may repeat x1) |
| Midazolam (if no IV access) | 0.2 mg/kg IM (max 10 mg) or 0.2 mg/kg intranasal | |
| Second-line | Levetiracetam | 60 mg/kg IV (max 4500 mg) over 15 min |
| Fosphenytoin | 20 mg PE/kg IV (max rate 150 mg PE/min) | |
| Valproic acid | 40 mg/kg IV (max 3000 mg) over 10 min | |
| Third-line (status epilepticus) | Continuous infusion: midazolam, propofol, or pentobarbital | Per status epilepticus protocol; continuous EEG monitoring required |
5. Coagulopathy in TBI
5.1 Trauma-Induced Coagulopathy (TIC) in TBI
TBI is uniquely associated with coagulopathy even in the absence of significant extracranial hemorrhage. The injured brain releases tissue factor and phospholipids that activate the extrinsic coagulation cascade, leading to a consumptive coagulopathy and hyperfibrinolysis. Up to 60% of patients with severe isolated TBI develop coagulopathy, which is an independent predictor of hemorrhage progression and poor outcome.10
Laboratory Markers:
| Test | Threshold of Concern | Action |
|---|---|---|
| INR | > 1.4 | Correct with FFP, PCC, or vitamin K |
| PTT | > 35 sec | Correct with FFP |
| Platelet count | < 100,000/μL | Transfuse platelets (goal > 100,000 in TBI) |
| Fibrinogen | < 200 mg/dL | Cryoprecipitate (10 units) or fibrinogen concentrate |
| Thromboelastography (TEG/ROTEM) | Abnormal parameters | Goal-directed component therapy |
5.2 Anticoagulant Reversal Protocols
Warfarin Reversal
| Agent | Dose | Onset | Notes |
|---|---|---|---|
| 4-Factor PCC (Kcentra) | INR 2–4: 25 units/kg; INR 4–6: 35 units/kg; INR > 6: 50 units/kg (max 5000 units) | 10–15 minutes | First-line agent. Fastest correction. Fixed-dose protocols (1500 units for all INR levels) are also used at some centers11 |
| Vitamin K (phytonadione) | 10 mg IV over 10–20 min | 4–6 hours for full effect | Always administer WITH PCC; PCC effect is temporary (6–8 hours) and vitamin K ensures sustained correction |
| FFP | 10–15 mL/kg | 30–60 minutes (includes thaw time) | Second-line if PCC unavailable. Volume overload risk. Incomplete correction |
Target: INR ≤ 1.4 within 60 minutes of presentation.
DOAC Reversal
| DOAC | Reversal Agent | Dose | Notes |
|---|---|---|---|
| Dabigatran (Pradaxa) | Idarucizumab (Praxbind) | 5 g IV (two 2.5 g vials) | Specific reversal agent; onset within minutes. If unavailable, use aPCC (FEIBA) 50 units/kg12 |
| Rivaroxaban, Apixaban, Edoxaban (Factor Xa inhibitors) | Andexanet alfa (Andexxa) | Low-dose: 400 mg bolus → 4 mg/min x 120 min; High-dose: 800 mg bolus → 8 mg/min x 120 min | Expensive; limited availability. High dose for rivaroxaban > 10 mg or apixaban > 5 mg taken within 8 hours13 |
| Rivaroxaban, Apixaban, Edoxaban (if andexanet unavailable) | 4-Factor PCC | 50 units/kg IV | Off-label but widely used. Reasonable alternative |
| All DOACs | Activated charcoal | 50 g PO | Only if DOAC ingested within 2–4 hours |
Antiplatelet Reversal
| Scenario | Recommendation | Evidence |
|---|---|---|
| Aspirin or clopidogrel with ICH | Platelet transfusion is NOT routinely recommended | The PATCH trial demonstrated that platelet transfusion in patients on antiplatelet agents with ICH was associated with WORSE outcomes (OR for death or dependence 2.05; 95% CI 1.18–3.56)14 |
| Aspirin with active surgical bleeding | Consider platelet transfusion or desmopressin (DDAVP) 0.3 mcg/kg IV | DDAVP may improve platelet function; limited evidence in TBI specifically |
| Dual antiplatelet therapy with expanding ICH | Case-by-case basis; consider DDAVP 0.3 mcg/kg | No high-quality evidence to guide management |
5.3 Tranexamic Acid (TXA) in TBI — CRASH-3 Trial
The CRASH-3 trial was a landmark international RCT (12,737 patients, 175 hospitals, 29 countries) evaluating TXA in acute TBI.15
CRASH-3 Protocol:
- Loading dose: 1 g IV over 10 minutes
- Maintenance dose: 1 g IV over 8 hours
- Within 3 hours of injury
Key Results:
| Finding | Detail |
|---|---|
| Primary outcome (head injury–related death) | Overall: OR 0.94 (95% CI 0.86–1.04) — not statistically significant for entire cohort |
| Mild-to-moderate TBI (GCS 9–15) | Significant benefit: RR 0.78 (95% CI 0.64–0.95). Head injury-related death reduced |
| Severe TBI (GCS 3–8) | No significant benefit |
| Time-dependent effect | Benefit strongest when administered within 3 hours of injury; no benefit after 3 hours |
| Safety | No increase in thrombotic events (PE, DVT, stroke, MI) |
| Patients with GCS 3 and bilateral unreactive pupils | Excluded from primary analysis (very high mortality regardless of treatment) |
Clinical Recommendation for TXA in TBI:
| Patient Group | Recommendation |
|---|---|
| GCS 9–15, intracranial hemorrhage on CT, within 3 hours | Administer TXA 1 g IV bolus + 1 g over 8 hours |
| GCS 3–8 with reactive pupils, within 3 hours | Consider TXA (potential benefit, not statistically proven) |
| GCS 3 with bilateral fixed pupils | TXA unlikely to benefit |
| > 3 hours from injury | Do NOT administer TXA |
| Isolated extracranial hemorrhage | Use per CRASH-2 protocol (different indication) |
6. Cerebral Herniation — Recognition and Emergency Management
6.1 Herniation Syndromes
| Syndrome | Mechanism | Clinical Features |
|---|---|---|
| Uncal (transtentorial) | Temporal lobe herniates through tentorial notch, compressing CN III and cerebral peduncle | Ipsilateral pupil dilation (CN III compression) → contralateral hemiparesis (cerebral peduncle compression) → progressive obtundation. Kernohan notch phenomenon: ipsilateral hemiparesis from contralateral peduncle compression against opposite tentorial edge (false localizing sign) |
| Central (descending transtentorial) | Bilateral downward herniation through tentorial notch | Bilateral small reactive pupils → bilateral fixed midpoint pupils → bilateral fixed dilated pupils. Progressive rostral-to-caudal deterioration. Cushing response (hypertension, bradycardia, irregular respirations) |
| Tonsillar (cerebellar) | Cerebellar tonsils herniate through foramen magnum, compressing medulla | Sudden respiratory arrest, cardiovascular collapse. May present with neck stiffness, head tilt. Often rapidly fatal |
| Subfalcine | Cingulate gyrus herniates under falx cerebri | Contralateral leg weakness (ACA compression); may progress to ACA infarction. Often clinically subtle |
| Upward (ascending transtentorial) | Posterior fossa mass pushes cerebellum upward through tentorial notch | Rapidly deteriorating consciousness, Parinaud syndrome (impaired upgaze), bilateral small pupils |
6.2 Cushing Response (Cushing Triad)
The classic triad of elevated ICP and impending herniation.16
| Component | Mechanism |
|---|---|
| Systemic hypertension (often severe, SBP > 200) | Brainstem reflex to maintain CPP against rising ICP |
| Bradycardia (often < 60 bpm) | Baroreceptor-mediated vagal response to hypertension |
| Irregular respirations (Cheyne-Stokes, ataxic, apnea) | Brainstem compression affecting respiratory centers |
Clinical Pearl: The full Cushing triad is a late and ominous sign. Hypertension alone may be the earliest component. Do not wait for the complete triad to initiate emergency treatment. Any new pupillary asymmetry > 1 mm or loss of pupillary reactivity in a TBI patient should be treated as herniation until proven otherwise.16
6.3 Emergency Management of Suspected Herniation
The following interventions are temporizing measures to buy time for definitive treatment (surgery or ICP-directed therapy). They should be initiated immediately upon clinical suspicion of herniation — do NOT wait for imaging confirmation.5 17
| Intervention | Details | Onset |
|---|---|---|
| Hyperosmolar bolus — 23.4% hypertonic saline | 30 mL IV bolus over 10–20 min via central line (can use peripheral for emergency if central line not available; risk of phlebitis) | Minutes |
| Hyperosmolar bolus — 3% hypertonic saline | 250 mL (5 mL/kg in children) IV bolus over 10–20 min via peripheral or central line | Minutes |
| Hyperosmolar bolus — Mannitol | 1 g/kg IV bolus (20% solution) over 15–20 min. Example: 70 kg patient = 350 mL of 20% mannitol | 15–30 min |
| Brief hyperventilation | Target PaCO2 30–35 mmHg (temporary bridge only — not sustained therapy). Use ETCO2 to guide | Seconds to minutes |
| Elevate HOB to 30° | Promotes venous drainage | Immediate |
| Ensure midline head position | Avoid rotation/flexion that impedes jugular venous drainage | Immediate |
| Ensure adequate MAP | Maintain SBP > 100–110 mmHg | Ongoing |
| Neurosurgical consultation | STAT for decompressive surgery evaluation | Immediate |
Key Distinction: Hypertonic saline is generally preferred over mannitol for acute herniation because: (1) it does not cause hypotension (mannitol is an osmotic diuretic), (2) it may be more effective at reducing ICP, and (3) it provides volume expansion rather than volume depletion.17
7. Temperature Management in Acute TBI
7.1 Fever Prevention
Fever (core temperature > 38°C / 100.4°F) is common after TBI and is associated with worse outcomes. Each degree of temperature elevation above 37°C is associated with increased ICP and worsened cerebral metabolism.18
| Recommendation | Detail |
|---|---|
| Target | Normothermia (36–37.5°C / 96.8–99.5°F) |
| Pharmacologic | Acetaminophen 650–1000 mg q6h (PO/PR/IV), ibuprofen 400–600 mg q6h if not contraindicated |
| Surface cooling | Cooling blankets, ice packs to groin and axillae |
| Intravascular cooling | Arctic Sun, Thermogard — if refractory to surface cooling |
| Avoid shivering | Buspirone 30 mg q8h, meperidine 25 mg IV PRN, skin counterwarming, magnesium sulfate 2–4 g IV |
7.2 Prophylactic Hypothermia
See Part 3 (Tier 3 ICP management) for detailed discussion of therapeutic hypothermia, including the Eurotherm3235 trial evidence.
8. Glucose Management
Hyperglycemia (> 180 mg/dL) is associated with worse outcomes after TBI, while hypoglycemia (< 70 mg/dL) is directly harmful to the injured brain. Tight glycemic control (80–110 mg/dL) is NOT recommended due to increased risk of hypoglycemia and cerebral energy crisis (demonstrated by cerebral microdialysis studies).19
| Parameter | Target |
|---|---|
| Blood glucose | 100–180 mg/dL |
| Avoid | Glucose > 200 mg/dL (treat with insulin infusion) |
| Avoid | Glucose < 70 mg/dL (associated with cerebral energy crisis) |
| Monitoring | Every 1–4 hours depending on insulin requirements |
9. Venous Thromboembolism Prophylaxis
TBI patients are at very high risk for VTE (DVT and PE) due to immobility, inflammation, and coagulopathy. The challenge is balancing VTE prevention against the risk of hemorrhage progression.20
| Recommendation | Detail |
|---|---|
| Mechanical prophylaxis | Intermittent pneumatic compression devices (IPCDs) — start on admission for ALL TBI patients |
| Pharmacologic prophylaxis | Low-molecular-weight heparin (enoxaparin 40 mg SQ daily) or unfractionated heparin (5000 units SQ q8–12h) |
| Timing of pharmacologic prophylaxis | Start 24–72 hours after injury if repeat CT shows stable hemorrhage. Earlier initiation (24 hours) appears safe for most patients with stable imaging.20 |
| Higher-risk patients | Those with large contusions, expanding hemorrhage, or post-craniotomy — delay pharmacologic prophylaxis until 48–72 hours with confirmed CT stability |
| Contraindication | Active intracranial hemorrhage expansion on serial imaging |
10. Nutrition
Early nutrition is associated with improved outcomes in severe TBI.5
| Recommendation | Detail | Evidence Level |
|---|---|---|
| Start enteral nutrition | Within 24–72 hours of admission | Level IIA |
| Caloric goal | Achieve full caloric replacement by Day 5 at the latest, preferably Day 7 | Level IIB |
| Route | Enteral preferred over parenteral | Level IIA |
| Protein target | 1.5–2 g/kg/day (TBI patients are hypermetabolic) | Expert recommendation |
| Gastric vs. post-pyloric | Start gastric; advance to post-pyloric if gastric intolerance | — |
11. Steroids — CONTRAINDICATED
Corticosteroids (methylprednisolone, dexamethasone) are contraindicated in moderate-to-severe TBI. This is one of the highest-level evidence recommendations in TBI management.21
CRASH Trial Evidence: The CRASH trial (MRC CRASH, 10,008 patients) demonstrated that high-dose methylprednisolone (2 g loading dose followed by 0.4 g/hour for 48 hours) significantly increased 14-day mortality (21.1% vs. 17.9%; RR 1.18; 95% CI 1.09–1.27) and 6-month mortality. This represents a Level I recommendation AGAINST steroid use in TBI.21
12. Initial Disposition and Transfer Decisions
12.1 Disposition by TBI Severity
| Severity | Disposition |
|---|---|
| Mild TBI (GCS 15), normal CT, no risk factors | May be discharged from ED after observation period (4–6 hours) with reliable companion and clear return precautions |
| Mild TBI (GCS 14–15), abnormal CT | Admit to monitored setting; serial neurologic exams q1–2h; repeat CT if clinical deterioration |
| Mild TBI (GCS 15), on anticoagulants | Admit for observation, repeat CT at 6–24 hours |
| Moderate TBI (GCS 9–12) | ICU or step-down admission; serial neurologic exams; neurosurgical consultation |
| Severe TBI (GCS ≤ 8) | ICU admission; ICP monitoring if indicated; neurosurgical consultation |
12.2 Transfer Criteria to Trauma Center / Neurosurgical Center
| Criterion |
|---|
| GCS ≤ 13 at any time after injury |
| Deteriorating neurological examination |
| Intracranial hemorrhage requiring potential neurosurgical intervention |
| Open or depressed skull fracture |
| Signs of basilar skull fracture |
| Penetrating head injury |
| Two or more proximal long bone fractures or pelvic fracture (polytrauma) |
| Need for ICP monitoring not available at the transferring facility |
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Sarode R, Milling TJ, Refaai MA, et al. “Efficacy and safety of a 4-factor prothrombin complex concentrate in patients on vitamin K antagonists presenting with major bleeding.” Circulation. 2013;128(11):1234-1243. DOI: 10.1161/CIRCULATIONAHA.113.002283 ↩︎
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Baharoglu MI, Cordonnier C, Salman RA-S, et al. “Platelet transfusion versus standard care after acute stroke due to spontaneous cerebral haemorrhage associated with antiplatelet therapy (PATCH): a randomised, open-label, phase 3 trial.” Lancet. 2016;387(10038):2605-2613. DOI: 10.1016/S0140-6736(16)30392-0 ↩︎
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