Head Injury

Background/Epidemiology

• Up to 1 million people attend A&E every year following head injury
  • 90% are mild/minor (GCS 13-15; likelihood of haematoma 1 in 3500)
  • 5% moderate (GCS 9-12; 1 in 50)
  • 5% severe (GCS 3-8; 1 in 7)
• For severe headaches, there is significant mortality
• The chance of a patient requiring surgery increases with disorientation and fracture:
  • No skull fracture + orientated – 1:6000
  • No skull fracture + disorientated- 1:200
  • Skull fracture + orientated – 1:32
  • Skull fracture + disorientated – 1:4

Pathophysiology

• Primary injury
  • Focal injuries
    • Scalp lesions (e.g. bruising; lacerations; bleeding; infection), Skull fractures (fissure fracture; skull base fractures, depression fractures etc).  Surface contusions and lacerations commonly affect the lateral hemispheres and the inferior surfaces of the temporal and frontal lobes due to their proximity with the skull and the common impact sites.  There are two possible areas of damage from one trauma: coup injury is injury nearest (or at) the site of trauma, whereas contre coup injury occurs at the diametrically opposite point- and is often more serious than coup injury.
  • Diffuse Axonal Injury
  • Concussion
    • brain injury associated with brief loss of consciousness (often seconds/minutes)
    • by definition there are no persisting neurological signs although many patients report lasting headache, impaired concentration, memory impairment and altered affect
  • Skull fracture
• Secondary Injury
  • These are, potentially, treatable events that may occur immediately or develop slowly e.g.
    • cerebral hypoxia
      • most brain injuries are further worsened by ischaemia/hypoxia
      • Hypoxia can cause cerebral oedema and rise in ICP, risking further ischaemia/hypoxia
      • common causes of hypoxia which may be possible to manage include
        • airway obstruction, alcohol/drug overdose, chest injury, aspiration pneumonia, central respiratory depression
    • intracranial haematoma;

Presentation

• NB If appropriate, go straight to ABCDE approach with C-spine
•  History
  • Ask about mechanism and site of injury
    • e.g. RTA (seatbelts, helmets, pedestrian, speed etc)
  • Ask about symptoms after (immediately and later) the injury
    • Crucial to ask about any loss of consciousness and amnesia (particularly retrograde)
• Examination
  • Full exposure/general exam for injuries and full neurological examination: Particular attention made to:
    • Level of consciousness (see GCS below) and behaviour
    • Pupil size and reactivity
    • Limb movements/power and responses (including coordination and tone)
• Referral should be considered in any patient with
  • GCS<15 on initial assessment;
  • any loss of consciousness as a result of injury;
  • any focal neurological deficit since the injury;
  • Any suspicion of a skull fracture or penetrating head injury;
  • Any amnesia (retro- or anterograde);
  • persistent or new onset headache since injury;
  • Any vomiting episodes since the injury;
  • Any seizures since the injury;
  • Any previous brain surgery, or brain injury;
  • Any history of bleeding or clotting disorders, or current anti-coagulant use;
  • current drug or alcohol intoxication
  • patients >65
  • suspicion of non-accidental injury in children

Immediate management (at the scene)

• ABCDE with C-spine management
• Analgesia

Assessment

• Glasgow Coma Scale
  • Eye opening
    • Spontaneous (4)
    • To verbal command (3)
    • To pain (2)
    • None (1)
  • Motor response
    • Obeys commands (6)
    • Localises pain (5)
    • Flexion withdrawal to pain (4)
      • NB to gauge this consistently, in general normal flexion to pain is usually tested by applying pressure under the supraorbital ridge- if the patient can lift their arm above the clavicle, this is regarded as ‘normal’ flexion response
    • Abnormal flexion- decorticate movement i.e. adduction of shoulder, internal rotation of shoulder; flexion of elbow; pronation of arm; flexion of wrists and fingers (3)
    • Abnormal extension- decerebrate movement i.e. extension of the arm and wrist (2)
    • None (1)
  • Verbal response
    • Orientated (5)
    • Confused conversation (4)
    • Inappropriate words (3)
    • Incomprehensible words (2)
    • None (1)

Investigations

• Imaging (CT first line as it is more sensitive for acute bleeding and more readily available)
  • Indications for CT within 1 hour

    • GCS <13 at any time since injury or <15 at 2 hours after injury; suspected skull fracture; post-traumatic seizure; focal neurological deficit; >1 episode of vomiting

  • Indications for CT within 8 hours (i.e. non immediate)
    • Anterograde amnesia (>30 minutes prior to event)
    • Any loss of consciousness/amnesia plus
      • >65 or dangerous mechanism of injury
    • Coagulopathy

Management

• Patients with GCS 15 and no risk factors for inpatient stay (e.g. intoxication- which can mask changes in consciousness caused by head injury) can be discharged with patient information
  • Similarly, patients with normal scans and quickly resolving GCS can be discharged (if suitable)
• Indication for admission include
  • Abnormal scan
  • GCS <15, regardless of imaging
  • When CT is indicated, but cannot be performed within appropriate time
  • Continuing signs e.g. headache, vomiting
  • Other concerns e.g. alcohol intoxication, other injuries, shock, suspected non-accidental injury; CSF leak; meningism
• In patients who have been admitted, but who are fully alert and no other reason to remain in hospital, can be discharge after 24 hours of observations
  • Minimal every 30 mins until GCS is 15
• Patients with moderate head injury should be assessed using ABCDE, with oxygen therapy to avoid hypoxia
  • AVOID morphine if possible as this can reduce the GCS inadvertently
• Patients with severe head injury (GCS 3-8) requires resuscitation and probably invasive ventilation
  • Immediate referral to neurosurgery is important (see neurosurgical/ITU management of head injury)
    • Other causes for neurosurgical referral include persisting coma (GCS <8) after resuscitation
    • Unexplained confusion for >4 hours
    • Deterioration in GCS after admission (particularly motor response)
    • Progressive focal signs
    • A seizure without full recovery
    • Definite/suspected penetrating injury
    • CSF leak

Further Intensive care management

• Sedation reduces cerebral metabolic rate, reduces cerebral blood flow and ICP.
• Ventilation maintains oxygenation and normocapnia.
  • Initially patients may be hyperventilated (short term <4hrs) to protect against brain damage.
• Management of BP, glucose and temperature are all crucial for head injury patients.
• If there is evidence of contusion but NO localising clinical signs- it is good to monitor ICP using intracranial bolt monitoring
• If there is evidence of bleeding and localising signs, a craniotomy or burr-hole procedure (craniotomy generally preferred) is often required for decompression.
• If there is no evidence of bleed/localising signs BUT evidence of raised ICP, IV mannitol may help relieve this (craniotomy may be required should localising signs appear)

Rehabilitation

• Neurological/Traumatic brain injury rehabilitation is vital for patients to regain function and independence.