Head Injury

Pathology

The aim of care is to prevent and treat secondary brain injury

  • Primary brain damage occurs at the time of the injury, manifests itself immediately, and is refractory to treatment. It is due to:
    • Diffuse axonal injury
    • Contusions
    • Lacerations of brain tissue
  • Secondary brain damage occurs after impact:
    • It is preventable
    • It is treatable.

Pathophysiology of secondary brain damage

  • Cytotoxic oedema
  • Microcirculation dysfunction, e.g. vasospam
  • Ischaemia, e. g. secondary to haematoma, oedema, contusion, and mass lesions >> increased ICP >>  decreased CPP >> global ischaemia

3 causes of secondary brain damage

  • Insufficient cerebral blood flow (i.e. decreased CPP, below 50mmHg is 90% death)
  • Insufficient substrate (i.e. hypoglycaemia, hypoxaemia)
  • Insufficient utilisation of substrate (i.e. cytotoxic neuronal damage)

Pressure-volume relationships of the cranial vault:

  • Volume components: 1800ml = 1500 + 150 + 150
    • 1500ml: brain parenchyma
    • 150ml: blood
    • 150ml: CSF
  • Small increases in volume are well-compensated
    • CSF is shunted via foramen magnum into spinal thecal sac
    • Venous blood is shunted out of the vault via the internal jugular veins/scalp veins
  • After these homeostatic mechanisms have been exhausted, the volume-pressure curve ‘takes off’

    Relationship between intracranial volume and pressure

ICP

  • Normal ICP is 0-10mmHg
  • Raised ICP in the trauma setting carries a bad prognosis
    • 0-20: 25%
    • >60: 100% mortality
  • Therefore it is wise to treat ICP above 20mmHg
  • Options for monitoring ICP
    • Ventricular catheter
      • Advantage: it is also therapeutic as the catheter can be used to drain CSF from the ventricles
      • Antibiotic and silver-impregnated catheters reduce infection risk
    • Fibreoptic transducer-tipped catheter
  • The main advantage of ICP monitoring is it allows you to identify sudden spikes in ICP early, before clinical signs like pupillary dilatation or the Cushing reflex may come into play
    • However, there is poor evidence to suggest that ICP-driven care is any better

Cerebral perfusion pressure

  • CPP = MAP – ICP
  • CPP should be maintained above 70mmHg.
  • It is usually kept constant
  • This autoregulation is dysfunctional in head injury

Cerebral blood flow

  • Determined by arterial Oxygen tension: hypoxia >> CBF increase
  • Determined by arterial CO2 tension: hypercapnia >> CBF increase
  • Therefore hypoventilation >> increased CBF >> cerebral oedema (cf altitude sickness)
  • Normal CBF: 55ml/100g/minute
  • Ischaemic threshold: 18ml/100g/minute
  • The CPP-CBF relationship is more sensitive in trauma
    • Normal CBF (55ml/100g/minute) could be maintained in a normal person with a CPP of 50mmHg
    • But a CPP of 50mmHg would be insufficient to maintain normal CBF in a head injury patient

Shifts and distortion

  • Expanding lesions >> ipsilateral ventricular compression and midline shift >> dilatation of contralateral lateral ventricle and obstruction of 3rd ventricle >> obstructive hydrocephalus >> raised ICP
  • Uncal herniation >> compression of IIIn. And posterior cerebral artery >> ipsilateral blown pupil and contralateral homonymous hemianopia

Trimodal distribution of death

  • Immediate
  • Hours (e.g. due to extradural or subdural haematoma)
  • Days-weeks (e.g. due to MOF and sepsis)

The most important time window is immediately after injury (before the second peak of death).

Investigation & Management

Immediate management: ABCDE following ATLS guidelines

  • Secure the airway, sedate, and paralyse early
  • Maintain BP > 90mmHg
  • Maintain PaO2 > 9kPa
  • Maintain PaCO2 3.5-4kPa
  • Document exact GCS early.

CT head must be performed immediately and analysed within 1 hour

Who to admit:

  • Anyone with GCS < 15
  • Any signs of raised ICP
    • Headache
    • Vomiting
  • Causes for concern
    • Distracting injuries
    • Meningism
    • NAI
    • CSF leak
  • CT abnormalities

GCS

  • Eyes: 4
    • 4: eyes open spontaneously
    • 3: eyes open in response to voice
    • 2: eyes open in response to pain
    • 1: eyes do not open
  • Verbal: 5
    • 5: alert and oriented
    • 4: confused, disorientated
    • 3: inappropriate words
    • 2: inappropriate sounds
    • 1: no sounds
  • Motor: 6
    • 6: obeys commands
    • 5: localises to painful stimuli
    • 4: flexion (withdrawal) response to pain
    • 3: abnormal flexor posturing, accentuated by pain (decorticate)
      • Above the red nucleus à rubrospinal tract flexes the elbows (like a stroke)
    • 2: abnormal extensor posturing, accentuated by pain (decerebrate)
      • Below the red nucleus
    • 1: no movement

Imaging:

  • XR
    • Lateral C-spine
    • Chest
    • Pelvis
    • Consider further spinal imaging
  • Indications for CT head in an adult
    • GCS<13
    • GCS<15 2 hours after injury
    • Suspected skull #
    • Seizure
    • Focal neurology
    • Vomiting >2
    • Pre-event amnesia >30 minutes before event
  • In anyone failing to recover in 24h or deteriorating, repeat the CT

Mannitol:

  • If there is a concern about coning – i.e. herniation of the cerebellar tonsils through the foramen magnum – give mannitol
  • IV 20% 200ml bolus of mannitol
    • Potential rebound decrease in CBF due to diuresis
    • Do not allow serum osmolality above 320 mOsm/L

Management of specific complications:

Skull fracture

  • Depressed
    • Consider surgery if
      • Significant mass effect
      • Underlying haematoma
    • Compound depressed/comminuted
      • Surgery = wound debridement and closure
        • If there is dural laceration à further surgery is required

Extradural haematoma

  • presents with a lucid interval
  • CT: Clear dural edge to haematoma
  • Management: craniotomy and evacuation of clot

Acute subdural haematoma

  • Results from more severe impact than EDH
  • More likely to present with coma than EDH
  • Two causes
    • Clot forms around parenchymal laceration
    • Tearing of the bridging veins
  • CT
    • Less defined edge
    • Effacement of ipsilateral ventricle
    • Midline shift
  • Treatment: craniotomy and evacuation of clot

Traumatic intracerebral haemorrhage

  • Often burst out of parenchyma into subarachnoid and subdural spaces
  • Extensive peri-haemorrhagic oedema >> raised ICP
  • Treatment: surgery
    • Surgery reduces the risk of deleterious consequences of raised ICP
    • But is unlikely to improve neurologic deficit

Chronic subdural haematoma

  • Epidemiology: generally occurs in 2 groups:
    • People likely to fall
      • Elderly
      • Epileptics
      • Alcoholics
    • People with cortical atrophy
      • Elderly
      • Alcoholics
      • Post-LP
  • Location: parietal most common. ¼ are bilateral.
  • Symptoms depend on size and location but can include:
    • Headache
    • Variable drowsiness in 1/3
    • Hemiparesis
  • CT: usually shows it. Not always
  • Management: surgery vs conservative
    • Surgery: uni/bilateral burr holes.
      • Possibly craniotomy for extensive clot.

CSF leak:

  • Occurs in about 2% of severe head injuries
  • Can appear years later
  • Types
    • Rhinorrhea (confirm with dipstick for glucose. B2-transferrin is another identifier)
      • Most are self-limiting within 1 month
      • RISK OF MENINGITIS
    • Otorrhea
      • Smaller/negligible risk of meningitis
      • Does not require repair, normally self-limiting

Traumatic aerocoele

  • Urgent repair is required if the aerocoele causes deterioration
  • Usually delayed dural repair is fine

Hydrocephalus

  • Traumatic hydrocephalus can be early or delayed:
    • Acute obstructive hydrocephalus can be due to:
      • Intraventricular haematoma
      • Posterior fossa haematoma obstructing 4th ventricle
    • Delayed communicating hydrocephalus is much more common
      • Due to subarachnoid blood >> communicating

Prognosis

Head injury can lead to a variety of long-term neurological sequalae depending on the severity of the injury and early complications. These sequalae include:

  • Cognitive deficit
  • Hemiparesis
  • Cranial nerve palsies
  • Carotico-cavernous fistulae (cavernous sinus syndrome)
  • BPPV (very common)
    • Detect with Dix-Hallpike
    • Treat with Epley or Semont
  • Post-traumatic amnesia
  • Cognitive impairment
  • Post-concussion syndrome
  • Epilepsy
  • Critical illness myopathy