Lucan · Conditions

"Head injury: extradural, subdural and concussion"

Australian guidance: EMST (RACS) Early Management of Severe Trauma + HealthPathways WA Head Injury and neurosurgical referral pathways + Concussion in Sport Australia (CISA) Position Statement 2023 + Canadian CT Head Rule (adopted into AU emergency department practice) + NICE Head Injury guideline (NG232, international benchmark cited alongside AU pathways)

1. Definition and epidemiology

Traumatic head injury spans a spectrum from concussion, a transient functional disturbance of the brain with no structural abnormality on standard imaging, through to extradural and subdural haematoma, focal collections of blood that compress the brain and can kill within hours if unrecognised. Head injury is one of the most common presentations to Australian emergency departments, and traumatic brain injury of any severity remains a leading cause of death and acquired disability in people under 45, alongside the rest of the polytrauma burden described elsewhere in this library. Falls dominate the mechanism in older Australians, particularly those on anticoagulant or antiplatelet therapy, while road trauma, assault, and sporting collisions dominate in younger adults; concussion specifically is heavily represented in contact and collision sports (Australian football, rugby codes, boxing), which is why Australia has a dedicated national sporting concussion framework rather than relying solely on general trauma guidance. Extradural haematoma (EDH) and acute subdural haematoma (SDH) are comparatively uncommon but disproportionately lethal, and distinguishing them clinically and radiologically, together with recognising when a "minor" head injury needs a CT scan at all, is the core skill this topic covers.

2. Pathophysiology

An extradural haematoma is arterial blood collecting between the inner table of the skull and the dura mater, classically from laceration of the middle meningeal artery as it runs in a groove on the inner surface of the temporal bone beneath the thin pterion; a linear temporoparietal skull fracture crossing this groove is the usual mechanism, so EDH is fundamentally a fracture-and-artery injury rather than a diffuse brain injury. Because the dura is tightly adherent to the skull at the cranial sutures, the expanding arterial haematoma is confined between suture lines, which is why EDH forms the classic biconvex, lens-shaped collection on CT and does not cross suture lines, though it can cross the midline. The textbook "lucid interval" describes initial loss of consciousness from the concussive impact, a period of apparent recovery as the patient wakes, then rapid deterioration in consciousness over minutes to a few hours as the arterial bleed expands and raises intracranial pressure; this pattern is a useful diagnostic clue when present but is seen in only a minority of confirmed EDH, so its absence never excludes the diagnosis.

Acute subdural haematoma is venous blood collecting between the dura and the arachnoid mater, arising from tearing of the bridging (cortical) veins that traverse this potential space to drain the cerebral cortex into the dural venous sinuses. These veins are torn by shearing, rotational acceleration-deceleration forces, which is why SDH is common after high-energy trauma but also after apparently trivial falls in the elderly, whose cerebral atrophy stretches the bridging veins across a wider subdural space and leaves them more vulnerable to shear; the same mechanism, combined with impaired clot formation, makes patients on warfarin, direct oral anticoagulants, or antiplatelet agents disproportionately represented. Because the venous bleed is not constrained by dural attachment to the skull, acute SDH spreads freely along the calvarial contour and forms a crescent-shaped, concave collection on CT that can cross suture lines but is limited at the midline by the falx cerebri. Acute SDH also differs from EDH in that it frequently coexists with direct parenchymal injury (cortical contusion, diffuse axonal injury) beneath the clot, so outcomes are often worse for a given clot volume than for isolated EDH. Chronic SDH is a distinct, slower process in which a small subacute bleed, often from a forgotten or minor injury weeks to months earlier, liquefies and becomes encased in a vascularised membrane that is itself prone to recurrent microhaemorrhage; it is a disease of the elderly and the anticoagulated, presenting insidiously with headache, cognitive decline, gait disturbance, or falls rather than an acute deficit, and appears hypodense or mixed-density (acute-on-chronic) rather than the uniformly hyperdense appearance of an acute bleed.

3. Clinical presentation and diagnostic criteria

The Glasgow Coma Scale (GCS) is the standardised bedside measure of conscious state and underpins every subsequent decision in this topic. It scores three domains: eye opening (4 spontaneous, 3 to voice, 2 to pain, 1 none), verbal response (5 orientated, 4 confused, 3 inappropriate words, 2 incomprehensible sounds, 1 none), and motor response (6 obeys commands, 5 localises pain, 4 normal withdrawal, 3 abnormal flexion/decorticate posturing, 2 extension/decerebrate posturing, 1 none), summed to a total of 3 to 15. Head injury severity is stratified as mild (GCS 13 to 15), moderate (GCS 9 to 12), and severe (GCS 8 or below); a GCS of 8 or less is the standard threshold for airway protection, reflecting loss of the ability to reliably protect the airway, consistent with EMST (RACS) teaching.

For the large majority of patients presenting with mild head injury, the decision to scan is guided by validated clinical decision rules, of which the Canadian CT Head Rule (CCHR) is the most widely taught and applied pattern in Australian emergency departments. The rule applies only to adults with GCS 13 to 15 after head trauma who have witnessed loss of consciousness, amnesia to the injury event, or witnessed disorientation; it excludes patients under 16 years, those without a clear history of head trauma as the amnesia or disorientation trigger, and those who have had a seizure after the injury, all of whom fall outside its evidence base and are managed on clinical grounds instead. High-risk criteria mandating CT (predicting need for neurosurgical intervention) are GCS below 15 at two hours post-injury, suspected open or depressed skull fracture, any sign of basal skull fracture, two or more episodes of vomiting, and age 65 or above; medium-risk criteria (predicting clinically important brain injury on CT) are retrograde amnesia of 30 minutes or more before impact and a dangerous mechanism, defined as a pedestrian struck by a vehicle, an occupant ejected from a vehicle, or a fall from a height of 3 feet (about 0.9 m) or five stairs or more. A critical caveat taught alongside this rule in Australian practice is that it was derived and validated in patients without a coagulopathy; anyone on warfarin, a direct oral anticoagulant, or dual antiplatelet therapy is scanned with a much lower threshold regardless of the CCHR score, per HealthPathways WA guidance, because anticoagulation both increases the risk of clinically significant bleeding and blunts the reliability of clinical decision rules derived in unanticoagulated cohorts.

Raised intracranial pressure (ICP) follows the Monro-Kellie doctrine: the skull is a rigid, fixed-volume container holding brain, cerebrospinal fluid, and blood, so any expanding mass (haematoma, oedema) can initially be compensated by displacing CSF and venous blood, but once this reserve is exhausted, ICP rises steeply for small further increases in volume. The Cushing response (or Cushing triad) — hypertension, bradycardia, and irregular respiration — is a late, ominous sign of critically raised ICP causing brainstem ischaemia, and typically precedes uncal or tonsillar herniation and death if untreated; a dilated, sluggish or fixed pupil ipsilateral to an expanding mass (from compression of the oculomotor nerve during uncal herniation) is an equally urgent bedside sign demanding immediate senior and neurosurgical involvement.

Basal skull fracture is diagnosed clinically as often as radiologically, through a cluster of delayed signs: Battle's sign (bruising over the mastoid process, typically appearing one to three days after injury, from a petrous temporal bone fracture), periorbital ecchymosis or "raccoon eyes" (bilateral bruising around the orbits, usually from an anterior fossa fracture), cerebrospinal fluid rhinorrhoea (from a fracture through the cribriform plate, sometimes demonstrated at the bedside by the "double ring" or halo sign when clear fluid mixed with blood separates into concentric rings on gauze), CSF otorrhoea and haemotympanum (from a petrous fracture), and cranial nerve VII or VIII palsy (facial weakness or hearing loss) when the fracture involves the facial canal or inner ear. Concussion, by contrast, produces no focal deficit or fracture: it presents with transient confusion, headache, dizziness, amnesia for the event, nausea, photophobia or phonophobia, and subtle cognitive slowing, typically without loss of consciousness, and by definition has a normal structural CT or MRI.

4. Investigations and AU-specific cutoffs

Non-contrast CT brain is the first-line and near-universal investigation once imaging is indicated by the criteria above, chosen for its speed and sensitivity for acute blood; MRI adds sensitivity for diffuse axonal injury and small chronic collections but is rarely first-line in the acute setting. Where a basal skull fracture is suspected but not obvious on CT, fine-cut bone-windowed imaging through the skull base improves detection, and where CSF leak is uncertain clinically, beta-2 transferrin assay on the fluid confirms a CSF fistula because beta-2 transferrin is found only in CSF and perilymph; it is typically a send-away reference-laboratory test with a multi-day turnaround in Australian practice, so it has no role in acute decision-making and is used to settle the diagnosis after the acute period. Cervical spine imaging is considered concurrently in any significant head injury, since the forces required to cause EDH, SDH, or diffuse axonal injury are frequently sufficient to injure the cervical spine, and spinal precautions are maintained until clearance per standard trauma protocols.

Serial neurological observation (GCS, pupils, vital signs) at defined intervals is the primary "investigation" for concussion and for patients discharged after a normal initial CT, since a small but real proportion of patients with an initially normal scan deteriorate from delayed haematoma expansion; HealthPathways WA and equivalent AU emergency protocols specify minimum observation periods and explicit written return-to-hospital advice before discharge. For patients on anticoagulation with a normal initial CT, a period of observation with a repeat scan several hours later is commonly practised locally, reflecting the recognised risk of delayed bleeding in this group even after an initially reassuring result.

5. Management

The primary survey (airway with cervical spine control, breathing, circulation, disability, exposure), taught under the EMST (RACS) framework, applies to every significant head injury and takes precedence over any imaging or definitive neurosurgical step. Secondary brain injury prevention is the guiding principle throughout: avoiding hypoxia (target oxygen saturation 94% or above) and hypotension (avoiding systolic blood pressure below 90 to 100 mmHg as a generic threshold, though current Brain Trauma Foundation guidance is age-stratified — target systolic blood pressure at or above 100 mmHg for age 50 to 69, and at or above 110 mmHg for age 15 to 49 or over 70) protects already-vulnerable brain tissue from compounding the primary insult, since a single episode of either has been repeatedly shown to worsen outcome in moderate to severe traumatic brain injury.

Uncomplicated mild head injury and concussion with a normal CT (where imaging was indicated) or a reassuring clinical picture not meeting scan criteria is managed conservatively: rest, simple analgesia, written head injury advice with explicit red-flag return precautions (worsening headache, vomiting, increasing drowsiness, new focal weakness, seizure), and a responsible adult to supervise the first 24 hours. Return-to-sport and return-to-learn for concussion follows a graded, stepwise protocol under the Concussion in Sport Australia (CISA) 2023 Position Statement: an initial period of relative rest until symptoms settle, followed by sequential stages of light aerobic activity, sport-specific exercise, non-contact training, and full-contact training, with a minimum of 24 hours symptom-free at each stage before progressing; children and adolescents are managed even more conservatively, with longer minimum timeframes and mandatory medical clearance before any return to contact training, reflecting Australian guidance around the small but catastrophic risk of second-impact syndrome in the paediatric and adolescent brain.

Any confirmed EDH or acute SDH triggers urgent neurosurgical consultation; in Western Australia, where neurosurgical services are centralised at Royal Perth Hospital and Perth Children's Hospital, this typically means urgent transfer coordinated through HealthPathways WA and RFDS Western Operations retrieval protocols for patients outside the metropolitan area. Surgical evacuation (burr hole or craniotomy) is generally indicated for an EDH with significant volume, midline shift, or associated neurological deficit, and for an acute SDH with clot thickness above roughly 10 mm or midline shift above roughly 5 mm, reflecting the accepted volumetric and shift thresholds used in neurosurgical decision-making; smaller, asymptomatic collections may instead be managed with close neurosurgical consultation and serial imaging. Measures to control acutely raised ICP while awaiting or alongside definitive surgery include head-of-bed elevation to around 30 degrees, loosening any constricting cervical collar strapping to avoid impeding venous drainage, maintaining normocapnia (with brief, controlled hyperventilation reserved as a temporising bridge in impending herniation), and hyperosmolar therapy with mannitol or hypertonic saline.

6. Pharmacology and AU PBS notes

Tranexamic acid, given intravenously within three hours of injury in patients with traumatic brain injury and intracranial bleeding, is supported by the CRASH-3 trial and has been incorporated into Australian trauma protocols alongside EMST teaching, reducing head-injury-related death without an appreciable increase in vascular occlusive events; this benefit was concentrated in patients with mild to moderate injury, and CRASH-3 showed no demonstrated mortality benefit, with a possible signal of harm, in patients presenting with a GCS of 3 or bilateral unreactive (fixed) pupils, so tranexamic acid is not given on the strength of this evidence in that subgroup. Where intracranial haemorrhage occurs in a patient on warfarin, urgent reversal with intravenous vitamin K and prothrombin complex concentrate (Prothrombinex-VF) is standard; for direct oral anticoagulants, idarucizumab reverses dabigatran specifically, while andexanet alfa (with limited Australian access) or, more commonly in practice, Prothrombinex-VF as a non-specific reversal agent is used for factor Xa inhibitors, guided by local protocols given variable PBS and hospital formulary access. Simple analgesia with paracetamol is preferred for head injury pain; NSAIDs and aspirin are avoided because of their antiplatelet effect and theoretical risk of promoting further bleeding. Seizure prophylaxis in severe traumatic brain injury is used selectively rather than routinely; where used, levetiracetam has largely superseded phenytoin in current Australian practice because of its more favourable interaction and monitoring profile, typically for a short course around the highest-risk early post-injury period. Hyperosmolar agents (mannitol 20% or hypertonic saline 3%) are used as above for acute ICP control rather than as a scheduled medication, and require monitoring of serum sodium and osmolality with repeated dosing.

7. Complications and monitoring

Untreated or delayed-treated EDH and acute SDH progress through the ICP-herniation pathway described above to coma and death, which is why rapid recognition and neurosurgical transfer, rather than any specific drug, remains the single most outcome-determining step in this topic. Chronic SDH carries its own risk of recurrent bleeding, sometimes prompting repeat burr hole drainage, and is a recognised, often under-recognised, cause of subacute cognitive decline or falls in older Australians that can mimic dementia if the antecedent (sometimes trivial or forgotten) head injury is not specifically asked about. Post-concussion syndrome, a constellation of persistent headache, dizziness, cognitive fog, and mood disturbance lasting weeks to months after an otherwise uncomplicated concussion, affects a meaningful minority of patients and is managed with graded return to activity, symptom-targeted therapy, and early involvement of concussion or rehabilitation services if symptoms persist beyond the expected window. Second-impact syndrome, catastrophic diffuse cerebral swelling triggered by a second head injury sustained before full recovery from a first concussion, is rare but disproportionately affects children and adolescents and underlies the conservative, stepwise return-to-sport timeframes in Australian concussion guidance. Repetitive concussion over a sporting career is the epidemiological substrate for chronic traumatic encephalopathy, a longer-term neurodegenerative concern that has driven much of the recent tightening of Australian sporting concussion protocols. Post-traumatic epilepsy risk rises with injury severity and is highest after depressed skull fracture, intracranial haematoma requiring evacuation, and prolonged loss of consciousness, and moderate to severe traumatic brain injury more broadly carries a substantial burden of ongoing cognitive, behavioural, and functional impairment that drives referral to dedicated brain injury rehabilitation services well beyond the acute admission.

Written for Australian practice and grounded in the guidance named above. Study material only — not medical advice. Always check against current guidelines.