Residency · Residency · Emergency Medicine

Traumatic Brain Injury: ED Management and Disposition

Classification

Severity by GCS

Traumatic brain injury is classified by Glasgow Coma Scale score. Mild TBI (GCS 13-15), which includes concussion, accounts for approximately 80 percent of all TBI. Moderate TBI (GCS 9-12) requires CT imaging and close monitoring. Severe TBI (GCS 3-8) requires intubation, intracranial pressure management, and neurosurgical consultation.

GCS Components and Limitations

The GCS assesses eye opening (1-4), verbal response (1-5), and motor response (1-6), and should always be reported by individual components (for example, E3V4M5 = 12). The motor component is the most predictive of outcome. The GCS has important limitations: it is confounded by intubation (verbal is scored as 1T), sedation, intoxication, facial swelling, and spinal cord injury. The scale was designed for repeated serial assessments rather than single snapshots.

Primary vs. Secondary Brain Injury

Primary injury refers to the direct mechanical damage at the time of impact — contusion, axonal shearing, and hemorrhage — which is not reversible. Secondary injury encompasses the ongoing cellular damage from hypoxia, hypotension, cerebral edema, seizures, inflammation, and fever that develops in the hours and days following the initial insult. ED management focuses entirely on preventing and treating secondary injury.

Intracranial Hemorrhage Patterns

Epidural Hematoma (EDH)

Epidural hematoma appears as a biconvex (lens-shaped) hyperdensity on CT, typically in the temporal region. It is usually arterial, resulting from a middle meningeal artery tear caused by a temporal bone fracture. The classic presentation includes a "lucid interval" of initial improvement followed by rapid deterioration — this is a surgical emergency. The collection does not cross suture lines because it is bound by dural attachments.

Subdural Hematoma (SDH)

Subdural hematoma appears as a crescent-shaped hyperdensity conforming to the brain surface. It results from bridging vein rupture caused by rotational or deceleration forces. Unlike epidural hematomas, subdural collections cross suture lines but do not cross the midline (falx). Acute SDH is hyperdense on CT, while chronic SDH is hypodense or mixed density. SDH is particularly common in elderly patients (whose brain atrophy stretches the bridging veins) and in anticoagulated patients.

Subarachnoid Hemorrhage (Traumatic)

Traumatic subarachnoid hemorrhage shows blood in the sulci and cisterns. It must be distinguished from aneurysmal SAH by mechanism, distribution pattern, and clinical context. It is usually managed conservatively, with monitoring for vasospasm in severe cases.

Intraparenchymal Hemorrhage / Contusion

Intraparenchymal hemorrhage occurs within the brain tissue, often at coup and contrecoup sites. The frontal and temporal poles are most vulnerable because they impact against bony ridges. Contusions can expand over 24 to 48 hours ("blossom"), so repeat imaging is indicated if there is clinical decline.

Diffuse Axonal Injury (DAI)

DAI is a shearing injury to white matter tracts from rotational acceleration and deceleration. CT may be normal or show only small petechial hemorrhages at the gray-white junction, corpus callosum, and brainstem. MRI (especially diffusion-weighted and susceptibility-weighted sequences) is far more sensitive. Severe DAI carries a poor prognosis.

CT Decision Rules

Canadian CT Head Rule (Adults)

The Canadian CT Head Rule applies to patients with GCS 13-15 who had loss of consciousness, amnesia, or witnessed disorientation. High-risk criteria (indicating the need for CT to evaluate for neurosurgical intervention) include GCS below 15 at 2 hours, suspected open or depressed skull fracture, signs of basilar skull fracture, two or more episodes of vomiting, and age 65 or older. Medium-risk criteria (for important brain injury on CT) include amnesia before impact exceeding 30 minutes and a dangerous mechanism. When applied correctly, the rule achieves 100 percent sensitivity for injuries requiring neurosurgical intervention.

PECARN Rule (Pediatric)

The PECARN rule stratifies children under 18 into risk groups based on age (under 2 years and 2 years and older). Children at very low risk (below 0.05 percent risk of clinically important TBI) can be safely observed without CT. Higher-risk children should receive CT. For children at intermediate risk, observation versus CT is based on shared decision-making with parents, clinical factors, worsening symptoms, physician experience, and parental preference.

ED Management of Severe TBI

Airway and Oxygenation

Intubation is required for GCS of 8 or below or inability to protect the airway. Avoiding hypoxia is paramount — SpO2 should be maintained above 94 percent because even a single episode of hypoxia doubles mortality. Rocuronium is commonly preferred for paralysis during RSI. The old concern about succinylcholine-induced ICP elevation is controversial and likely minimal. Ketamine, previously considered contraindicated due to ICP concerns, has been debunked as unsafe — it is safe and hemodynamically favorable for TBI intubation.

Blood Pressure Management

Hypotension (SBP below 90) doubles mortality in TBI. The target is SBP above 100 mmHg per Brain Trauma Foundation guidelines. Vasopressors (norepinephrine) should be used if needed after volume resuscitation. Permissive hypotension is contraindicated in TBI — the brain requires adequate perfusion pressure.

ICP Management

Head of Bed Elevation

The head of the bed is elevated to 30 degrees to promote venous drainage. Midline head position is maintained to avoid jugular venous compression from head rotation.

Hyperosmolar Therapy

Mannitol at 0.5 to 1 g/kg IV bolus (20 percent solution) acts as an osmotic diuretic, drawing fluid from brain parenchyma. Its onset is 15 to 30 minutes, but it can cause hypotension from diuresis, requiring adequate volume status. Hypertonic saline — 23.4 percent (30 mL bolus via central line) or 3 percent (250-500 mL bolus) — does not cause hypotension because it expands intravascular volume. The 3 percent concentration can be given peripherally. Hypertonic saline is preferred in hemodynamically compromised patients. Target serum osmolality should remain below 320 mOsm/L for mannitol, and serum sodium below 160 mEq/L for hypertonic saline.

Seizure Prophylaxis

Levetiracetam (1000-2000 mg IV) or phenytoin (20 mg/kg IV) is given for the first 7 days after severe TBI to reduce early post-traumatic seizures (within 7 days). This prophylaxis does not prevent late post-traumatic epilepsy. Levetiracetam is increasingly preferred because it has fewer drug interactions and does not require level monitoring.

Avoiding Secondary Insults

Normothermia must be maintained because fever worsens secondary injury and should be treated aggressively. Hyperglycemia should be avoided with a glucose target of 80 to 180 mg/dL. Hyperventilation (PaCO2 below 35) causes cerebral vasoconstriction and ischemia and must be avoided except as a brief temporizing measure for acute herniation, when PaCO2 is transiently lowered to 30-35. In the absence of herniation, PaCO2 should be maintained at 35 to 45 mmHg. Euvolemia should be maintained throughout.

Signs of Herniation

A unilateral fixed, dilated pupil indicates ipsilateral uncal herniation compressing cranial nerve III. The Cushing triad — hypertension, bradycardia, and irregular respirations — is a late finding. Posturing progresses from decorticate (flexor, with upper extremity flexion) to decerebrate (extensor, with upper extremity extension) to flaccid. Emergent treatment includes hyperosmolar therapy, brief hyperventilation, and consideration of emergent surgical decompression.

Anticoagulant Reversal in TBI

Warfarin is reversed with 4-factor PCC (Kcentra) at 25 to 50 IU/kg plus vitamin K 10 mg IV, targeting an INR below 1.4 within 30 minutes. For DOACs, idarucizumab reverses dabigatran, and 4-factor PCC is used for factor Xa inhibitors (with andexanet alfa if available). Platelet transfusion for antiplatelet agents is not routinely recommended, as the PATCH trial showed worse outcomes. Anticoagulation should be reversed before CT if clinical suspicion for intracranial hemorrhage is high — reversal should not be delayed for imaging.

Mild TBI and Concussion

Assessment

Most patients with GCS 15 and a negative CT will have good outcomes. Concussion is a clinical diagnosis characterized by headache, amnesia, confusion, dizziness, and nausea — CT is typically normal. Post-concussive symptoms including headache, cognitive difficulties, sleep disturbance, and emotional changes can persist for weeks to months.

Disposition

Patients with a negative CT, GCS of 15, and a reliable observer at home can be safely discharged with head injury precautions. Written return precautions should address worsening headache, vomiting, confusion, seizure, weakness, and abnormal behavior. Anticipatory guidance about post-concussive symptoms should be provided. Follow-up with primary care or a concussion specialist within 1 to 2 weeks is appropriate.

<image>A CT head image panel showing four types of intracranial hemorrhage. Panel A: Epidural hematoma with a biconvex hyperdense collection in the temporal region, bounded by suture lines, with midline shift. Panel B: Acute subdural hematoma with a crescent-shaped hyperdense collection over the left cerebral convexity, crossing suture lines, with midline shift and sulcal effacement. Panel C: Traumatic subarachnoid hemorrhage with hyperdensity in the sylvian fissures and basal cisterns. Panel D: Intraparenchymal contusions with hemorrhagic areas in the frontal and temporal lobes bilaterally (coup-contrecoup pattern). Each panel is annotated with arrows and labels identifying the hemorrhage type and key diagnostic features.</image>

<image>An infographic showing the PECARN pediatric head injury decision algorithm for children under 2 years and children 2 years and older. Each age group has a flowchart starting with GCS assessment, then evaluating for high-risk and intermediate-risk criteria. High-risk features lead to CT recommended. Intermediate-risk features lead to a shared decision-making zone with options for CT or observation. Low-risk (no criteria present) leads to observation without CT. Key criteria are listed for each age group with estimated ciTBI risk percentages at each decision node.</image>

<image>A management algorithm for severe TBI in the ED showing the sequential steps from arrival to disposition. The pathway includes: simultaneous ABCDE assessment with cervical spine protection, RSI intubation (with drug choices labeled), blood pressure targets (SBP greater than 100), immediate CT head, assessment for surgical lesion, ICP management steps (head elevation, osmotherapy, seizure prophylaxis, temperature control, ventilation targets), herniation protocol (mannitol or HTS bolus, brief hyperventilation, emergent neurosurgery), and disposition to OR or ICU. Targets for PaCO2 (35-45), SpO2 (greater than 94%), glucose (80-180), and temperature (36-37.5 degrees C) are displayed in a sidebar.</image>

Clinical Pearls

A single episode of hypotension (SBP below 90) doubles mortality in TBI — maintaining cerebral perfusion pressure aggressively is non-negotiable. Permissive hypotension is contraindicated in TBI, making it the critical exception to damage control resuscitation in polytrauma. Ketamine is safe for TBI intubation — the old teaching about ICP elevation is debunked. Do not routinely hyperventilate TBI patients — PaCO2 below 35 causes cerebral vasoconstriction and worsens ischemia, and brief hyperventilation is reserved only for acute herniation. Hypertonic saline is preferred over mannitol in hypotensive patients because it does not cause diuresis-related hypotension. Anticoagulation should be reversed immediately in anticoagulated patients with head trauma — do not wait for the CT result. In children, PECARN allows safe observation without CT for low-risk head injuries, reducing unnecessary radiation exposure. Epidural hematoma can present with a "lucid interval" — any head-injured patient who initially improves then deteriorates needs emergent CT and neurosurgical consultation.

References

• Carney N, et al. Brain Trauma Foundation: Guidelines for the Management of Severe Traumatic Brain Injury. 4th ed. Neurosurgery. 2017;80:6-15.
• Kuppermann N, et al. PECARN: Identification of children at very low risk of clinically important brain injuries. Lancet. 2009;374:1160-1170.
• Stiell IG, et al. The Canadian CT Head Rule for patients with minor head injury. Lancet. 2001;357:1391-1396.
• Badjatia N, et al. Guidelines for prehospital management of TBI. Prehosp Emerg Care. 2008;12(Suppl 1):S1-S52.
• 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;394:1713-1723.

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