Traumatic Brain Injury: Intracranial Hematomas & Concussion
Read the shape on CT, time the surgery, and know when to bench the athlete.
Initial assessment and imaging
Glasgow Coma Scale. Eye (1–4), verbal (1–5), and motor (1–6) scores sum to 3–15: mild TBI 13–15, moderate 9–12, severe 3–8. A GCS of 8 or less means the airway is unprotected — intubate.
Who needs a CT. Noncontrast head CT is the first study because it rapidly shows blood, fractures, and mass effect. For minor head injury with loss of consciousness, amnesia, or disorientation, the Canadian CT Head Rule lists high-risk features — GCS below 15 two hours after injury, suspected open or depressed fracture, signs of basilar skull fracture (hemotympanum, raccoon eyes, Battle sign, CSF leak), two or more episodes of vomiting, and age 65 or older — plus medium-risk features (retrograde amnesia ≥30 minutes, dangerous mechanism). Patients on anticoagulants were excluded from the rule; they, and those on antiplatelet drugs, deserve a low threshold for imaging.
Intracranial blood in an anticoagulated patient is an emergency: reverse immediately (4F-PCC plus IV vitamin K for warfarin, idarucizumab for dabigatran, 4F-PCC for factor Xa inhibitors, since andexanet alfa was withdrawn from the US market in December 2025).
Epidural and subdural hematomas
Epidural hematoma. A blow to the temple fractures the thin temporal bone at the pterion and lacerates the middle meningeal artery, a branch of the maxillary artery. Arterial blood peels the dura off the inner table, forming a hyperdense biconvex (lentiform) collection limited by sutures, where the dura is firmly attached, although it can cross the midline. The classic brief loss of consciousness, lucid interval, and rapid decline occurs in only a minority. Expansion causes uncal herniation: an ipsilateral dilated pupil from oculomotor nerve compression and contralateral hemiparesis from pressure on the cerebral peduncle. Symptomatic or large collections need emergent craniotomy, with excellent outcomes if surgery is prompt; small ones in alert patients without deficits can be followed with serial CT in a neurosurgical center.
Acute subdural hematoma. Shearing forces tear bridging veins crossing from the cortex to the dural sinuses. Brain atrophy (older age, chronic alcohol use) stretches these veins and anticoagulation magnifies bleeding; in infants, subdural blood with retinal hemorrhages suggests abusive head trauma. CT shows a hyperdense crescent that crosses sutures but stops at the falx and tentorium. Evacuate if the clot is thicker than 10 mm or shifts the midline more than 5 mm regardless of GCS, or if a comatose patient's GCS falls by 2 or more points or the pupils become asymmetric or fixed; otherwise observe in the ICU, reverse anticoagulation, and repeat CT. Prognosis is worse than for epidural hematoma because the underlying brain is injured.
Chronic subdural hematoma. Weeks after a minor or forgotten fall, an older, alcohol-using, or anticoagulated patient develops headache, fluctuating confusion, gait disturbance, or mild hemiparesis — easily mistaken for dementia, delirium, or stroke. The collection is isodense to brain at roughly 1–3 weeks (look for effaced sulci and midline shift, or obtain MRI) and hypodense afterward. Symptomatic collections are drained through burr holes; recurrence is common, and dexamethasone worsened outcomes in a randomized trial.
| Feature | Epidural | Acute subdural | Chronic subdural |
|---|---|---|---|
| Source | Middle meningeal artery | Bridging veins | Bridging veins; fragile membranes rebleed |
| Typical patient | Young adult, blow to the temple | Elderly, alcohol use, anticoagulants; shaken infant | Elderly after a trivial fall |
| Course | Lucid interval, then rapid decline | Often impaired from the start | Weeks of fluctuating confusion and headache |
| CT | Hyperdense biconvex; stops at sutures | Hyperdense crescent; crosses sutures | Hypodense crescent |
| Treatment | Emergent craniotomy | Craniotomy if >10 mm or shift >5 mm | Burr-hole drainage if symptomatic |
Contusion and diffuse axonal injury
Contusions. The brain bruises where it strikes the skull (coup) and on the opposite side as it rebounds (contrecoup), most often at the inferior frontal lobes and anterior temporal poles, which scrape over the irregular floors of the anterior and middle cranial fossae. Hemorrhagic contusions characteristically enlarge and swell over 24–72 hours, so any neurologic decline warrants repeat CT. Orbitofrontal injury often shows up as disinhibition and personality change rather than weakness.
Diffuse axonal injury. Rotational acceleration–deceleration in high-speed crashes shears axons throughout the white matter. The hallmark is immediate, prolonged coma out of proportion to a CT that is normal or shows only a few petechial hemorrhages. MRI with susceptibility-weighted or gradient-echo sequences reveals punctate hemorrhages at the gray–white junction, the corpus callosum (especially the splenium), and, in the worst cases, the dorsolateral brainstem. There is no surgical target, and many patients remain severely disabled.
Severe TBI: preventing secondary injury
The primary injury occurs at impact; management prevents secondary injury from hypoxia, hypotension, raised intracranial pressure, seizures, fever, and hyperglycemia.
| Parameter | Target | Why |
|---|---|---|
| Airway | Intubate if GCS ≤8 | Protect airway, control ventilation |
| Oxygenation | SpO2 >90% | Hypoxia worsens outcome |
| Blood pressure | SBP ≥100–110 mm Hg | A single hypotensive episode markedly raises mortality |
| PaCO2 | 35–45 mm Hg | Hyperventilate only briefly for herniation |
| ICP | Treat if >22 mm Hg | Monitor in salvageable patients with abnormal CT |
| CPP (MAP − ICP) | 60–70 mm Hg | Maintains cerebral blood flow |
ICP control. An external ventricular drain both measures ICP and drains CSF. Add head elevation to 30° with the neck neutral, sedation and analgesia, and mannitol or hypertonic saline; decompressive craniectomy is reserved for refractory pressure. Hyperventilation lowers ICP through vasoconstriction but also reduces cerebral blood flow, so it is only a brief bridge.
Proven and disproven therapies. Phenytoin (the trial evidence) or, commonly, levetiracetam for 7 days lowers early post-traumatic seizures but does not prevent late epilepsy. Corticosteroids increased mortality in the CRASH trial and are contraindicated; prophylactic hypothermia and sustained hyperventilation do not help. In CRASH-3, tranexamic acid given within 3 hours reduced head injury–related deaths in mild to moderate TBI.
Concussion and its consequences
Diagnosis. Concussion is a transient, trauma-induced disturbance of brain function: headache, confusion, amnesia, dizziness, nausea, light sensitivity, slowed thinking, and mood or sleep changes. Most patients never lose consciousness, and CT and MRI are normal; imaging is reserved for red flags such as worsening headache, repeated vomiting, seizures, focal deficits, or declining consciousness.
Return to learn and play. A suspected concussion means removal from play with no same-day return. After 24–48 hours of relative rest (light daily activity is encouraged; strict rest in a dark room is counterproductive), the patient climbs symptom-limited stages of at least 24 hours each, stepping back if symptoms recur:
- Return to learnRebuild school workload with temporary accommodations.
- Light aerobic exerciseWalking or stationary cycling.
- Sport-specific and non-contact drillsAdd complexity and resistance, no head impact.
- Full-contact practiceOnly when symptom-free and medically cleared.
- Return to competitionNormal game play.
Children and adolescents recover more slowly and are advanced more conservatively.
Second impact syndrome. A second blow before recovery from a first concussion can abolish cerebral autoregulation and cause malignant brain swelling with herniation within minutes. It is rare, mainly affects adolescents, and is often fatal — the central reason symptomatic athletes never return to play.
Post-concussion syndrome. Headache, dizziness, poor concentration, irritability, insomnia, and depression can persist for weeks to months. Treat with graded activity, headache care that avoids analgesic overuse, vestibular or cognitive rehabilitation, and management of mood symptoms.
Chronic traumatic encephalopathy. Repetitive head impacts, as in contact sports, can lead years later to a progressive tauopathy with mood and behavioral change, memory loss, dementia, and parkinsonism; the diagnosis is confirmed only at autopsy by phosphorylated tau deposits at the depths of cortical sulci.