Introduction

Epidemiology

  • 6-10 deaths per 100,000 per annum
  • 70% male
  • 40% children

Presentation

  • 90% mild (GCS ≥13)
  • 10% moderate (GCS 9-12) and severe (GCS ≤8)

Cause

  • Most common = fall and assault, followed by road traffic accident
  • Alcohol involved in up to 65% of cases
  • The introduction of seat belt regulation, air bag, crash helmet and alcohol control have prevented many severe head injuries.

 

      Pathology

      Impact damage – often unavoidable

           1) Cortical contusion and laceration

      • Cortical contusion = bruising on the brain, commonly affecting the frontal and temporal lobes.
      • Especially common at the under or opposite the site of impact (contra-coup)

           2) Diffuse axonal injuries

      • Disruption and tearing of axons form the mechanical shearing following deceleration.

       

      Secondary brain damage – occurs after initial injury, may be preventable

           1) Intracranial haematoma

      • Extradural (27%): Bleeding of the middle meningeal artery into the extradural space
      • Subdural (26%): Rupture of the bridging veins from cortical surface to the venous sinus
      • Intracerebal ± subdural (38%)
      • Extra ± intradural (8%)

           2) Cerebral swelling

      • From vasodilation and oedema

           3) Tentorial or tonsillar herniation

      • Supratentorial haematoma → Increasing ICP → Midline shift → Lateral tentorial herniation (Herniation of the medial temporal lobe) → Midbrain compression and damage
      • Uncontrolled lateral tentorial herniation ± Diffuse bilateral hemispheric swelling → Central tentorial herniation
      •  Central tentorial herniation → Tonsillar herniation (Herniation of the cerebellar tonsils through the foramen magnum) → Brainstem compression

           4) Cerebral ischaemia

      • Hypotension + Increased ICP → Reduced cerebral perfusion
      • Reduced cerebral perfusion ± Hypoxia → Cerebral ischaemia

           5) Infection

      • Skull fracture → Dural tear → Meningitis ± Cerebral abscess
      • Seldom within 48 h of injury
      • Meningitis may develop after months or years

      Assessment and Immediate Management

      Airway – Any obstruction? Is it maintained? Oropharynheal airway needed?Cervical spine – Is immobilization needed?Breathing – Administer oxygen. Is respiratory movement adequate?Circulation – Is there hypotension or tachycardia? Large bore cannula and IV fluid. Take blood including group and save/cross matchDisability – Pupils equal and reactive to light? GCS or AVPU? Consider intubation if GCS ≤ 8.Exposure/Everything else

      • Chest: Flail segment, haemo/pneumothorax
      • Abdomen: Bleeding (Pain, tenderness, rigidity, bruising)
      • Head and spine: Focal deficits, conscious level
      • Limbs: Lacerations and fractures

       

      History for head injury

      • Mechanism of injury
      • Duration of loss of consciousness
      • Duration of post-traumatic amnesia
      • Presence of headache or vomiting
      • Presence of seizure
      • Cause and circumstances of injury

       

      Examination of head injury

      • Sign of depressed fracture of the skull

           - Explore deep laceration with a gloved finger

      • Sign of basal skull fracture

           - CSF otorrhoea or rhinorhoea. Clear fluid from the ear or nose. Dipstick test reveals glucose

           - Bilateral periorbital haematoma. Black eyes with no associated damage around the eyes

           - Subconjuctival haemorrhage extending to the posterior limit of the sclera

           - Battle’s sign. Brusing over mastoid.

      • Conscious level
      • Pupillary response

           - Medial temporal lobe herniation through the tentorial hiatus compresses the occulomotor nerve (III) → Dilated pupil with impaired or absent reaction to light on the ipsilateral side of lesion

      • Focal neurological deficits

           - Signs of upper motor neuron lesions from limb examination. Increased tone, decreased power, brisk reflexes, upgoing extensor plantar, impaired coordination

           - Cranial nerve palsy.

      Glasgow Coma Scale (GCS)

      Motor response

           6 – Obey command

           5 – Localize pain

           4 – Withdraw from pain

           3 – Abnormal flexion to pain

           2 – Abnormal extension to pain

           1 – No movement

      Vocal response

           5 - Orientated

           4 - Confused speech

           3 - Inappropriate words

           2 - Incomprehensible sound

           1 – No sound

      Eye opening

           4 - Spontaneously

           3 - To voice

           2 - To pain

           1 - No eye opening

       

      Generally head injuries are classified as follows:

      • Severe GCS≤ 8
      • Moderate GCS 9 - 12
      • Minor GCS ≥ 13

         

        Further Management

        Further management aims to prevent secondary brain damage

        • Ensure that airway is patent and blood oxygenation is adequate. Hypoxia worsens cerebral damage.
        • Urgent evacuation of space occupying haematoma. If conscious level deteriorates, consider mannitol.
        • Monitor intracranial pressure (ICP) and blood pressure (BP) to maintain adequate cerebral perfusion pressure (CPP). CPP = Mean BP – ICP
        • Anticonvulsants if seizure occurs
        • Surgical repair of persisting dural defect

         

        C-spine immobilization until full risk assessment including clinical assessment ± imaging for:

        • GCS ≤ 15 on initial presentation
        • Neck pain or tenderness
        • Focal neurological deficit
        • Parasthesia in the extremities
        • Any clinical suspicion of cervical spine injury

         

        Any other clinical suspicion of cervical spine injury CT within an hour for:

        • GCS ≤ 13 on initial assessment in the emergency department;
        • GCS ≤ 15 at 2 hr after the injury;
        • Suspected open or depressed skull fracture;
        • Any sign of basal skull fracture;
        • ≥ 1 episode of vomiting in adult; ≥ 3 episodes of vomiting in children;
        • Post-traumatic seizure;
        • Coagulopathy (eg clotting disorder, warfarin) + some loss of consciousness or amnesia; or
        • Focal neurological deficit

         

        CT within 8 hour (or immediately if present ≥ 8hr after injury) for:

        None of the above indication (for CT within an hour) and either:

        • Amnesia for ≥ 30mins before impact;
        • Age ≥ 65 years + some loss of consciousness or amnesia; or
        • Some loss of consciousness or amnesia + dangerous mechanism of injury, for example

             - A pedestrian struck by a motor vehicle

             - ejected from motor vehicle

             - fall from a height greater than 1m or 5 stairs

        CT Diagnoses Not To Be Missed

        Extradural haematoma Subdural haematoma

        Outcomes after Head Injury

        Outcomes after severe head injury

        • Predicted by the initial GCS and the duration of coma
        • Residual disability physically (hemiparesis, dysphasia, epilepsy) and mentally (intellect, memory, behaviour)
        • Most recovery occurs in the first 6 months. Physiotherapy and occupational therapy are important in the process of rehabilitation.
        • 40% eventually back to normal. ≤ 2% vegetative state with no awareness or ability to communicate with the environment.

         

        References

        1. Lindsay KW, Bone I, Callander R. Neurology and neurosurgery illustrated, 4th ed. Churchill Livingstone, Edinburgh, 2004.

        2. National collaborating centre for acute care. Head injury: Triage, assessment, investigation and early management of head injury in infants, children and adults. NICE, September 2007.

         

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