1.6 Traumatic Brain Injury

Question 1

A 54-year-old patient is admitted to the Emergency Department following a traumatic brain injury.
A CT scan reveals only cerebral oedema.

a) What is secondary brain injury and when is it likely to occur? (2 marks)

Answer 1

Primary brain injury occurs due to the initial insult, depends on the nature, intensity and duration of impact.

Macroscopically: fracture, contusion, haematoma, cerebral oedema, diffuse brain injury.

Microscopically: cell wall disruption, increased membrane permeability disrupting ionic haemostasis.

Secondary brain injury is the deleterious changes that happen over hours to days in the brain as a consequence of the initial injury, mediated by
inflammatory, neurogenic and vasogenic processes.

Question 2

b) Outline the main physiological and cellular changes associated with secondary brain injury. (7 marks)

Answer 2

1. > > Primary injury
   (due to e.g. intracerebral bleeding)
   may exhaust the compensatory capacity of the brain,

leading to a raised ICP.
Initially, as one component in the closed
compartment of the cranium increases in size,
it is compensated for by a reduction in another component (intravascular blood or CSF).

This is the Monroe–Kelly doctrine.

Ultimately, this compensation will reach its limit and ICP will start to rise.

This results in cerebral ischaemia and hypoxia.

2. Inflammation**
   » Inflammation and local tissue damage
   cause excessive release of
   excitatory neurotransmitters (excitotoxicity),
   resulting in calcium influx to cells,
   cell oedema and death.
3. Mediators
   » Dying cells release mediators
   (platelet activating factor, leukotrienes,
   oxygen free radicals)
   that affect blood vessel permeability,

resulting in vasogenic fluid accumulation,

raising ICP further,

contributing to hypoperfusion,
cerebral ischaemia,
and neurodegeneration.

4. > > Loss of cerebral autoregulation
   exacerbates cerebral oedema and raised ICP.
5. Hypes

> > Hypoxia, hypotension, hyper- or hypocapnia and hyper- or hypoglycaemia will exacerbate secondary brain injury,
worsen ability to autoregulate, cause direct changes to brain tissue size and therefore impact on ICP and perfusion, thus perpetuating a downward vicious cycle.

6. > > Seizures

will cause increased ICP,
exacerbating poor cerebral perfusion if untreated.

Seizures will also lead to raised PaCO2
and reduced PaO2,

which will further decrease the brain’s
autoregulatory capacity and
increase its metabolic demand.

Question 3

c) How can secondary brain injury be minimised in this patient? (11 marks)

Answer 3

1. Airway:
   » Intubate and control ventilation if:
   • Unable to protect own airway.
   • Loss of laryngeal reflexes.
   • GCS less than 8.
   • Hypoxic.
   • Hypercarbic.
   • Seizures.

> > Cervical spine control with airway management: immobilise if there is possibility of injury but ensure that collar does not obstruct venous return.

2. Respiratory:

> > Target PaO2 greater than 13 kPa, PaCO2 4.5–5.0 kPa.

> > PEEP to maintain oxygenation, ideally less than 15 cm H2O.
Oxygen saturation and etCO2 monitoring.

3. Cardiovascular:

> > Cannulate.

> > Maintain mean arterial pressure (MAP)
greater than 80 mm Hg
(higher if ICP is raised)
using isotonic fluids and
vasopressors as necessary.
Guide with intra-arterial blood pressure (BP) monitoring.

> > Head neutral, tube ties not too tight, 15–30 degree head-up tilt to optimise venous return.
Paralyse if coughing/straining on tube.

> > Catheterisation to guide fluid balance.

4. Neurological:

> > Target cerebral perfusion pressure >60 mm Hg,
ICP less than 20 mm Hg
(if have capabilities of monitoring in this hospital).

> > Sedate adequately to reduce CMRO2.

> > Treat seizures.

> > Maintain blood glucose 6–10 mmol/l.

> > Treat any raised temperature (which raises CMRO2).

> > Manipulation of ICP spikes:
• Temporising measures:
hyperventilation, mannitol 0.25–1 g/kg, 5%
hypertonic saline 2 ml/kg
(keep Na less than 155 mmol/l, plasma
osmolality less than 320 mOsm/l).

• Definitive: discuss with neurosurgical unit
if ongoing coma,
ongoing confusion,
seizures without recovery,
progressive neurological abnormality;
consider transfer for decompressive craniectomy
or other neurosurgical intervention.

5. Exposure, environmental control:
   » Seek other injuries causing blood loss, which may make maintaining MAP or haemoglobin at adequate levels for brain perfusion a proble``.

Question 4

CPP goal

ICP goal

Answer 4

> > Target cerebral perfusion pressure >60 mm Hg,
ICP less than 20 mm Hg
(if have capabilities of monitoring in this hospital).