Traumatic Brain Injury


See Traumatic Brain Injury Guideline for management

Minor GCS 13-15
Moderate 9-12
Severe 3-8

RTAs young people
Falls elderly

Assoc with severe morbidity even if minor

Classification

  • Penetrating or blunt
  • Isolated or other injuries
  • Primary (outside our control) or secondary (at which Rx is aimed)
GCS
Most common method of assessing injury
Motor score most predictive
Doesn’t take other features into account

Pathophysiology

Cerebral contusions
Areas of ‘bruising’ within the brain tissue with relatively localized cellular damage, haemorrhage and oedema
May be large haemorrhagic regions or small ‘point’ contusions
Outcome will depend on location and size along with pressure effects that they may generate locally
Maximal swelling and bleeding is often not seen until up to 72 h after the initial insult
Diffuse axonal injury
Shown by loss of grey/white differentiation on CT
Caused by widespread shearing forces that occur as the brain undergoes stresses such as rapid deceleration.
SAH
Tearing of an intracranial vessel
As for non-traumatic SAH, traumatic SAH may be associated with vasospasm.
Epidural or subdural haematomata
Occur frequently after trauma; and if bilateral, the associated localizing signs may be absent.
Epidural haematomata may have relatively little underlying associated ‘brain damage’; although if of sufficient size, brain compression and ischaemia may occur. Early evacuation is generally associated with a good outcome.
Subdural haematomata, because of the involvement of brain tissue, have a much worse prognosis.
Surgical evacuation will usually be performed if there is evidence of any mass effect or increased intracranial pressure (ICP) to which the haematoma may be contributing.
Transfer
Indications
  • Severe head injury or focal signs (whether or not they need neurosurgical intervention)
  • Needing ventilation, ICP monitoring, or both.
  • Should be optimised prior to transfer which should occur within 4h

Management

Good evidence for specific treatment strategies is lacking
Remember 5 goals - normotension, normoxia, normocapnia, normothermia and normoglycaemia.
See guideline for Traumatic Brain Injury

Additional neuroprotective agents

Ca antagonists
Nimodipine improves outcome in non-traumatic SAH
No outcome benefit in trials for traumatic SAH
Magnesium
Neuroprotective in animals with traumatic or ischaemic injury if given within 1st 24h
Steroids
High dose methylpred → ↑ mortality (CRASH trial)
Other
Antioxidants and excitatory amino acid antagonists have shown no benefit in trials

Monitoring

ICP monitors
Used to guide CPP targets and maintain ICP <20

Indications
  • Severe head injury (GCS <9) with an abnormal admission CT scan
  • Normal CT and 2 or more of
  • Age >40
  • Hypotension
  • Abnormal posturing

Types of monitor
Epidural catheter
Subdural bolt or catheter
- Prone to blocking
- Less infection risk than interventricular
Intraventricular catheters
- The most accurate
- Can be used to drain CSF
- Infection risk
Intraparenchymal catheter

Lundburg waves
A
Sustained pressure waves 60-80 every 5-20 mins
Life threatening due to cerebral vasodilatation in response to ↓ blood flow
B
Small (10-20), short lasting every 30-120s
Fluctuations in CBV
C
Small oscillations reflecting changes in BP

Jugular venous oximetry
Varies with the ratio of cerebral oxygen consumption to CBF and is normally 60–70%
Low values imply ischaemia and high values suggest hyperaemia

Transcranial Doppler (TCD) ultrasound
Measures blood flow velocity in major cerebral arteries.
The most commonly imaged artery is the middle cerebral artery

Secondary problems

Diabetes insipidus

Cranial DI is caused by post-traumatic failure of ADH secretion
Signs
  • Polyuria (>3000ml/24h or >125mls/h)
  • Hypernatraemia
  • Urine osmolarity <300 mOsmol/l, rises > 50 % after desmopressin (DDAVP)
  • Serum osmolarity>300 mOsmol/l
Management:
  • If diuresis <4000 ml /24 h then only fluid replacement
  • If diuresis >4000 ml /24 h then fluid replacement + DDAVP 2 mcg i.v.
  • Correct hypovolaemia with Hartmanns, then use Glucose 5 % for correction of hypernatraemia.
  • Plasma sodium lowering not faster than 0.7 mmol/h.(16.8 mmol/day)

SIADH
Signs
  • Hyponatraemia
  • Normovolaemia (without peripheral oedema)
  • Urine sodium level >25mmol/l
  • Serum osmolality <280 mOsmol/l
  • Urine osmolality >serum osmolality
Therapy:
  • Fluid restriction (1000 ml isotonic fluid/24 h)
  • If fluid restriction alone fails or hyponatraemia <115 mmol/l
  • NaCl 3 % + frusemide
  • Aim for slow serum sodium correction (max 1 mmol/h, 12/24h) to avoid myelinolysis.
Cerebral Salt Wasting Syndrome (CSW)
Signs
  • Hyponatraemia
  • Hypovolaemia
  • Urine sodium levels >50 mmol/l
Therapy
  • Fluid replacement with saline 0.9 %
  • NaCl 3 % if necessary for slow serum sodium correction

Be aware - high glucose, triglyceride or albumin levels can fake a hyponatraemia (pseudohyponatraemia)