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ukmla 2026

Head Injury and Traumatic Brain Injury

Injury to the head from trauma — severity assessed by GCS. CT head indications, tranexamic acid for moderate-severe TBI, and neurosurgical referral criteria are defined by NICE NG232

Review date
reviewed 2026-04-05
Reading time
7 min read
Author
Dr Kola Tytler MBBS CertHE MBA MSt MRCGP
Emergency Medicinecommonacute
On this page
Condition details
Emergency Medicine
common
7 min read
reviewed 2026-04-05
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About This Page

This is a clinician-written, evidence-based summary aligned to the 2026 MLA Content Map. It is intended for medical students and junior doctors preparing for the UKMLA. Always cross-reference with NICE guidance, local protocols, and clinical judgement.

Key points

  • Assess with GCS (3–15). Mild TBI: GCS 13–15. Moderate: 9–12. Severe: 3–8. GCS ≤8 = intubate and protect airway
  • CT head within 1 hour if: GCS <13 on assessment, GCS <15 at 2 h, suspected skull fracture, post-traumatic seizure, focal neurology, >1 episode vomiting, amnesia >30 min before impact (adults)
  • CT head within 8 hours if: on anticoagulants/antiplatelets (excluding aspirin monotherapy) with no other CT indication — or shared decision if risk-benefit discussed (NICE NG232)
  • Tranexamic acid 1 g IV within 2 hours: for suspected moderate/severe TBI (GCS ≤12) — even without extracranial bleeding (CRASH-3)
  • Extradural haematoma: lucid interval then rapid deterioration. "Lens-shaped" on CT. Neurosurgical emergency
  • Subdural haematoma: crescent-shaped on CT. Acute (trauma) or chronic (elderly, anticoagulated, trivial injury)

Overview

Head injury encompasses any trauma to the head that may or may not result in traumatic brain injury (TBI). TBI is classified as mild (GCS 13–15), moderate (GCS 9–12), or severe (GCS 3–8). Primary brain injury occurs at the moment of impact (contusion, diffuse axonal injury, haemorrhage). Secondary brain injury develops subsequently from hypoxia, hypotension, cerebral oedema, raised intracranial pressure, and infection — prevention of secondary injury is the focus of emergency management. Intracranial haemorrhage types include extradural (between dura and skull — usually middle meningeal artery), subdural (between dura and arachnoid — bridging veins), subarachnoid, and intracerebral. NICE NG232 (2023) provides comprehensive UK guidance on assessment, CT imaging criteria, and management.

Epidemiology

Approximately 1.4 million people attend UK emergency departments with head injury annually. The majority (~90%) are mild. TBI is the leading cause of death and disability in young adults (15–45 years). Falls are now the most common mechanism (especially in elderly), followed by road traffic collisions and assaults. Males are affected 2–3× more frequently. Alcohol intoxication is a factor in approximately 30–50% of head injury presentations and complicates assessment. Elderly patients on anticoagulants are at increased risk of intracranial haemorrhage even from minor injury.

Clinical Features

Symptoms
Headache (common but non-specific)
Loss of consciousness (even brief = significant — warrants assessment)
Amnesia: retrograde (before event) or anterograde (after event). >30 min retrograde amnesia = CT indication
Vomiting (>1 episode in adults = CT indication)
Confusion or disorientation
Post-traumatic seizure
Deterioration after initial improvement (lucid interval — think extradural haematoma)
Signs
GCS <15 — assess and document EACH component (Eye, Verbal, Motor)
Focal neurological deficit (pupil asymmetry, hemiparesis, cranial nerve palsy)
Signs of skull fracture: periorbital bruising (raccoon eyes), mastoid bruising (Battle sign), CSF otorrhoea/rhinorrhoea, haemotympanum
Cushing triad (raised ICP): hypertension + bradycardia + irregular respirations — late and ominous sign
Fixed dilated pupil (ipsilateral to lesion — uncal herniation compressing CN III)
Scalp laceration, haematoma, deformity, palpable fracture

Investigations

First-line
GCS assessmentBest Eye (1–4) + Verbal (1–5) + Motor (1–6) = total 3–15. Reassess regularly
CT head (non-contrast)Within 1 h: GCS <13, GCS <15 at 2 h, suspected skull fracture, post-traumatic seizure, focal neurology, >1 vomit, retrograde amnesia >30 min (adults), dangerous mechanism. Within 8 h: anticoagulants/antiplatelets (shared decision per NICE NG232)
Second-line
CT cervical spineFor all patients with suspected C-spine injury (see Canadian C-spine Rule / NICE NG232 criteria)
Clotting screenIf on anticoagulants or suspected coagulopathy — INR, APTT, platelets
Blood glucoseHypoglycaemia can mimic head injury. Also: baseline U&Es, FBC
Specialist
CT angiographyIf vascular injury suspected (skull base fracture, penetrating injury)
MRI brainSubacute phase: more sensitive for diffuse axonal injury, small contusions
ICP monitoringNeurosurgical ICU — for severe TBI (GCS ≤8) or deteriorating patients. Target ICP <22 mmHg

Management

NICE NG232 (Head injury: assessment and early management), 2023
1
Pre-hospital and initial ED management
  • ABCDE approach. Cervical spine immobilisation if mechanism warrants
  • GCS assessment — serial monitoring. GCS ≤8 → intubate and ventilate (protect airway)
  • High-flow oxygen. Avoid hypotension (target systolic >90 mmHg adult — brain needs perfusion)
  • TXA 1 g IV within 2 h for suspected moderate-severe TBI (GCS ≤12), even without extracranial bleeding (NICE NG232)
  • Urgent CT head as per NICE criteria (see investigations)
2
Management of specific intracranial injuries
  • Extradural haematoma: neurosurgical emergency — craniotomy for evacuation. "Talk and die" scenario if missed
  • Acute subdural haematoma: craniotomy if significant mass effect/midline shift. High mortality (~50%)
  • Chronic subdural: burr hole drainage. Often elderly/anticoagulated with gradual confusion/unsteadiness
  • Traumatic SAH: manage conservatively if mild. May need ICP monitoring and neurosurgical intervention if severe
  • Depressed skull fracture: surgical elevation if depressed >table thickness or open/contaminated
  • Diffuse axonal injury: supportive ICU care. No surgical option — prognosis depends on severity
3
Raised ICP management
  • Head elevation 30° (aids venous drainage)
  • Avoid: hypotension, hypoxia, hyperthermia, hypercarbia (all worsen ICP)
  • Osmotherapy: IV mannitol 20% (0.25–1 g/kg) or hypertonic saline 3–5% for acute ICP crises
  • Sedation and analgesia (propofol + fentanyl) — reduces cerebral metabolic demand
  • Target ICP <22 mmHg, CPP 60–70 mmHg
  • Decompressive craniectomy: if refractory raised ICP despite medical management (RESCUE-ICP trial)
4
Anticoagulant reversal
  • Warfarin + intracranial haemorrhage: IV vitamin K 5 mg + 4-factor prothrombin complex concentrate (PCC, e.g. Beriplex). Target INR <1.5 within 1 h
  • DOAC + intracranial haemorrhage: idarucizumab for dabigatran. Andexanet alfa or PCC for factor Xa inhibitors
  • Do NOT delay CT for reversal — but reverse as soon as intracranial haemorrhage confirmed
5
Discharge and follow-up
  • Discharge with written head injury advice (NICE): return if worsening headache, persistent vomiting, confusion, seizure, limb weakness, clear fluid from ear/nose
  • Responsible adult to observe for 24 h
  • Post-concussion syndrome: headache, dizziness, cognitive difficulties, mood changes — may persist weeks to months. Refer if persisting at 4 weeks
  • Be aware of pituitary dysfunction post-TBI — may present days to months later

Complications

  • Raised ICP and herniation: Expanding haematoma or cerebral oedema → transtentorial (uncal) herniation → fixed dilated pupil, hemiparesis, death if untreated
  • Post-concussion syndrome: Headache, dizziness, cognitive and mood disturbance persisting weeks to months after mild TBI
  • Post-traumatic epilepsy: Seizures developing after TBI — risk highest with penetrating injury, intracranial haemorrhage, early seizures
  • Pituitary dysfunction: Can occur acutely or months post-TBI — anterior pituitary hormone deficiencies (GH, cortisol, gonadotrophins, TSH)
  • CSF leak: From skull base fracture — rhinorrhoea or otorrhoea. Risk of meningitis. Most resolve spontaneously
  • Chronic subdural haematoma: Develops weeks after initial injury (often trivial) — particularly in elderly and anticoagulated patients
UKMLA Exam Tips
  • 1NICE NG232 CT criteria: GCS <13, GCS <15 at 2 h, suspected skull fracture, post-traumatic seizure, focal neuro, >1 vomit. LEARN THESE
  • 2Extradural haematoma: "lens-shaped" (biconvex) on CT. Usually middle meningeal artery. Lucid interval → rapid deterioration. NEUROSURGICAL EMERGENCY
  • 3Subdural haematoma: "crescent-shaped" on CT. Bridging veins. Acute = trauma; chronic = elderly, anticoagulants, trivial injury
  • 4TXA 1 g IV within 2 h for moderate-severe TBI (GCS ≤12) — CRASH-3. Even without extracranial bleeding
  • 5Battle sign (mastoid bruising) + raccoon eyes (periorbital bruising) = skull base fracture. CSF leak risk
  • 6Cushing triad: hypertension + bradycardia + irregular respiration = raised ICP. Late and ominous. Act immediately
  • 7Anticoagulant reversal: warfarin = vitamin K + PCC. Dabigatran = idarucizumab. DO NOT DELAY

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Verified Sources & References

NICE NG232 — Head injury: assessment and early management
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