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Head injury

SNOMED: 82271004992 wordsUpdated 03/03/2026
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Exam Tips

  • In OSCEs, state and perform ABCDE first, then document GCS as components (E, V, M) not just total score.
  • Always mention cervical spine protection in potentially significant mechanisms until injury is excluded.
  • Basal skull fracture signs (CSF leak, periorbital bruising, Battle sign, haemotympanum) are high-yield red flags for urgent CT and specialist referral.
  • Anticoagulant use after head trauma is a key exam trigger for lower threshold imaging and possible reversal discussions.
  • For concussion counselling, examiners expect advice on graded return to activity and strict safety-net symptoms requiring urgent reassessment.
  • See Figure: GCS scoring table and Figure: common intracranial bleed patterns on CT (extradural lens-shaped vs subdural crescentic) in standard emergency medicine texts.

Definition

Head injury is any trauma to the head excluding isolated superficial facial injury, and ranges from minor scalp trauma to severe intracranial damage. Traumatic brain injury (TBI) is present when the injury causes disturbance of normal brain function (for example altered consciousness, amnesia, or focal deficit), and is commonly graded as mild, moderate, or severe using Glasgow Coma Scale (GCS).

Pathophysiology

Head injury causes a primary insult (impact-related skull/scalp injury, contusion, diffuse axonal injury, or intracranial bleeding) followed by secondary injury from hypoxia, hypotension, cerebral oedema, excitotoxicity, inflammation, and raised intracranial pressure that reduce cerebral perfusion. Bleeding patterns include extradural, subdural, subarachnoid, and intraparenchymal haemorrhage; mass effect and herniation risk rise as intracranial volume increases. Concussion reflects transient neuronal dysfunction without necessarily showing structural changes on CT. Neuroendocrine dysfunction (including post-traumatic hypopituitarism) may occur after moderate/severe TBI and can present later with non-specific symptoms. See Figure: Glasgow Coma Scale eye/verbal/motor framework and Figure: Monro-Kellie doctrine schematic (standard neurotrauma texts).

Risk Factors

  • High-energy mechanism (fall >1 m or >5 stairs, high-speed road traffic collision, ejection/rollover, diving injury, motorized recreational vehicle or bicycle collision)
  • Anticoagulant therapy (for example warfarin, apixaban, rivaroxaban, dabigatran) or known bleeding disorder
  • Older age and frailty
  • Alcohol or drug intoxication (may both increase injury risk and obscure assessment)
  • Previous head injury or pre-existing neurological disease
  • Safeguarding risk (non-accidental injury, domestic abuse, self-harm context)
  • Risk factors for prolonged post-concussive symptoms: female sex, age >40, comorbid anxiety/depression, poor social support

Clinical Features

Symptoms

  • Loss of consciousness
  • Confusion or disorientation
  • Amnesia (retrograde or anterograde)
  • Headache
  • Vomiting
  • Seizure
  • Dizziness and poor concentration (common in concussion)
  • Visual disturbance (including diplopia)
  • Neck pain

Signs

  • Reduced or fluctuating GCS
  • Focal neurological deficit (weakness, speech disturbance, sensory changes, gait/balance problems)
  • Pupillary asymmetry or poor light reactivity
  • Signs of basal skull fracture (CSF leak from nose/ear, periorbital ecchymosis, Battle sign, haemotympanum)
  • Scalp/skull trauma
  • Hypoxia or shock physiology (tachycardia, hypotension, prolonged capillary refill)
  • Midline cervical spine tenderness or inability to rotate neck 45 degrees left and right
  • Fundoscopic signs such as papilloedema (if present)

Investigations

Serial Glasgow Coma Scale and neurological observations:Deterioration in GCS, new focal signs, or persistent abnormal mental state suggests evolving intracranial pathology and need for urgent escalation
Urgent non-contrast CT head (ED pathway):May show skull fracture, extradural/subdural/intracerebral haemorrhage, subarachnoid blood, contusion, oedema, or mass effect; can be normal in concussion
CT cervical spine (or plain films in selected pathways):Identifies associated cervical fracture/dislocation when neck injury risk factors are present
Bedside observations and capillary blood glucose:Detects hypoxia, hypotension, or hypoglycaemia as contributors to reduced consciousness
Blood tests (FBC, U&E, coagulation profile, group and save where indicated):Supports detection of anaemia/coagulopathy/electrolyte disturbance and informs reversal or perioperative planning

Management

Lifestyle Modifications

  • Immediate safety-netting and urgent transfer to emergency care if red flags are present (reduced GCS, focal deficit, seizure, suspected skull fracture, repeated vomiting, worsening headache, anticoagulant use with concern for bleed)
  • Follow trauma ABCDE approach and protect cervical spine when injury mechanism or examination suggests possible neck injury
  • For uncomplicated concussion, advise 24-hour responsible adult supervision, physical/cognitive rest for 24-48 hours, then graded return to study/sport/work as symptoms permit
  • Avoid alcohol, sedative recreational drugs, driving, cycling, and contact sport until clinically recovered and medically cleared
  • Provide clear return precautions: seek urgent care for drowsiness, confusion, repeated vomiting, severe/worsening headache, seizure, weakness, visual or speech change

Pharmacological Treatment

Analgesia (first line)

  • Paracetamol 1 g orally every 4-6 hours when required (maximum 4 g/day) in adults
  • Child: paracetamol 15 mg/kg every 4-6 hours (maximum 4 doses in 24 hours; do not exceed age/weight BNF limits)

Preferred initial analgesic after head injury. Avoid accidental overdose from combination products; use caution in severe hepatic impairment or low body weight.

Antiemetic (if clinically needed after assessment)

  • Cyclizine 50 mg orally/IM/IV up to three times daily
  • Ondansetron 4 mg orally or IV every 8 hours as required

Use the lowest effective dose; avoid masking neurological deterioration with excessive sedation. Check QT-risk factors with ondansetron.

Seizure treatment in acute traumatic brain injury (specialist/emergency setting)

  • Lorazepam 4 mg IV, may repeat once after 10-20 minutes if seizure continues
  • If no IV access: midazolam 10 mg buccal
  • Second-line specialist loading often uses levetiracetam 60 mg/kg IV (max 4.5 g) or phenytoin 20 mg/kg IV

Do not use routine prophylactic antiepileptics for all minor head injuries. Manage airway and breathing concurrently.

Anticoagulant reversal when intracranial haemorrhage is suspected/confirmed

  • Warfarin reversal: intravenous vitamin K (for example 5 mg) plus 4-factor prothrombin complex concentrate (dose per INR/local protocol)
  • Dabigatran reversal: idarucizumab 5 g IV
  • Factor Xa inhibitor reversal: andexanet alfa where indicated/available or PCC per local major haemorrhage protocol

Time-critical specialist decision; balance thrombosis risk against life-threatening bleed risk.

Early haemorrhage-modifying therapy in moderate/severe TBI (major trauma pathway)

  • Tranexamic acid 1 g IV over 10 minutes, then 1 g IV over 8 hours (ideally within 3 hours of injury)

Used in selected patients under trauma protocols; delayed administration beyond the early window is less beneficial.

Surgical / Interventional

  • Neurosurgical evacuation of extradural or subdural haematoma when indicated
  • Decompressive craniectomy for refractory raised intracranial pressure in selected severe TBI
  • Repair of depressed skull fracture or penetrating injury where appropriate
  • Insertion of intracranial pressure monitoring and neurocritical care support

Complications

  • Intracranial haemorrhage (extradural, subdural, subarachnoid, intracerebral)
  • Skull fracture and associated cranial nerve injury
  • Post-traumatic seizures/epilepsy
  • Raised intracranial pressure, herniation, and death
  • Persistent post-concussion symptoms (headache, dizziness, cognitive slowing)
  • Hypopituitarism with possible sodium dysregulation or adrenal crisis
  • Cognitive impairment, behavioural change, depression, anxiety, and PTSD
  • Communication/swallowing and mobility deficits causing long-term disability

Prognosis

Most people with minor head injury recover fully, and overall mortality among ED presentations is low (around 0.2%). Poor outcomes are concentrated in moderate-to-severe injuries (GCS 12 or less), especially with impaired consciousness or intracranial bleeding. Persistent symptoms after mild TBI usually improve over 2-3 months, while delayed serious deterioration after an initially mild presentation is uncommon and very late deterioration is rare.

Sources & References

🏥BMJ Best Practice(1)

💊BNF Drug References(25)

NICE Guidelines(1)

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