TRAUMATIC BRAIN INJURY

- Blunt injury
- Penetrating injury

Mechanism of Injury
Nature of the brain makes it susceptible to acceleration and deceleration injury:
- Soft, gel-like in consistency, one part of the brain may move in relation to another.
- Surrounded by CSF and vascular compartments make it floats within the skull.
At the moment of impact, there is sudden deceleration (or acceleration), that causes
displacement and distortion of the cerebral tissue.
Injury to the brain tissue at the time of impact can be:
-

Functional loss.
Structural injury to the neurons.
Temporary or permanent.
The extent of the injury can be generalised or localised.

A) Primary Injury
= Injury to the brain tissue at the time of impact.
- Structural damage: Bruises, oedema, shearing damage to nerve cells,
haemorrhage from tearing of small vessels.
- Functional loss: Generalised (Loss of consciousness) or localised (focal
neurological deficit). Functional loss can be temporary or permanent.
- Terms loosely used to describe brain injury:
o Concussion: generalised, temporary physiological paralysis results in a
transient loss of consciousness. No structural damage.
o Contusion: loss of consciousness with bruises or oedema of the brain.
o Laceration LOC, intracerebral bruises and brain surface is torn.

B) Secondary Injury
= Injury caused by processes that are activated subsequent to the primary injury.

Respiration
o Inadequate ventilation
o Hypercarbia and hypoxia
o Venous congestion and cerebral oedema.

Systemic blood pressure and blood volume

o Pressure and volume of systemic blood affect blood flow to the brain.
o In normal circumstances, cerebral auto regulatory mechanism maintain cerebral
blood flow despite changes in systemic blood pressure.
o In brain injury the mechanism is impaired, thus falls in systemic volume or
pressure likely result in cerebral ischemia.

Intravenous fluid
o Low plasma osmolality may result in intravascular fluid being drawn into the brain
tissue and worsens brain swelling.
o Disturbance of the blood-brain barrier.
o Fluid given must be isotonic.
o SIADH may cause hyponatremia.

Temperature
o Raise in body temperature increases tissue metabolic demand.
o This in turn may aggravate cellular failure or aggravate manifestation of poor
function.

Brain swelling
o Tissues (including brain) reacts to insult e.g. ischemic, inflammatory or traumatic,
by swelling due to oedema.
o Fluid accumulation is both extracellular and intracellular.
o Disturbance in the permeability of capillary and cellular membrane.
o Generalised throughout one or both lobes.
o Causes increase in intracranial pressure.

Intracranial haematoma

Extradural haematoma
Fracture of the temporal or parietal bone.
Anterior or posterior branch of the middle meningeal artery.
More common in children and young adults.
Typically presents as short LOC, followed by lucid interval and again drop in
conscious level.

The latter is due to gradual enlarging haematoma that causes raised ICP and
supratentorial herniation.

Symptoms:
Deterioration in conscious level.
Lucid interval.

Signs:
Bruise or boggy swelling in the temporal region.
Pupil dilatation on the side of haematoma.
Hemiparesis on the same side of the haematoma.

Subdural haematoma
Injury to bridging vessels that travel between skull and brain.
Concave or crescent shape.
The force of injury is more severe.

Intracerebral haematoma

Extradural Haematoma

Subdural Haematoma

Subarachnoid Haematoma

Intracerebral Haematoma

Presentation of Intracranial haematoma

-

Loss of consciousness
Altered conscious level
Amnesia
Headache
Vomiting without nausea
Focal neurological deficit
Seizure
Lucid interval

Raised Intracranial Pressure

= An increase in the pressure inside the skull.
Monro-Kellie hypothesis:
- The cranium is incompressible thus, any increase in volume of one of the cranial
constituents must be compensated by a decrease in volume of another.
Symptoms:
- Headache
- Vomiting without nausea
- Altered level of consciousness
- Ocular palsies
Signs:
- Pupillary dilatation
- Abducens nerve palsy
- Cushings triad: High SBP, widened pulse pressure, bradycardia and abnormal
breathing.
- Abnormal respiratory pattern: Cheyne-Stokes respiration is rapid breathing for a
period and then absent for a period, occurs because of injury to the cerebral
hemispheres or diencephalon. Hyperventilation can occur when the brainstem or
tegmentum is damaged.
Fundoscopy:
- Papilledema.

Treatment:
- Adequate oxygenation
- Hyperventilation:

- Release of hard collar.

- Head up position.
- IV Mannitol
- Analgesia and sedation.
- EVD.
- Decompressive craniectomy.

Management
1) Primary survey
- Primary survey and provide the necessary action.
- Cervical collar: All patients with head injury should be assumed to have a
simultaneous cervical spine injury until proven otherwise. Thus cervical collar to
all, unless no neck pain, no tenderness, full ROM and no neurological deficit.
- Monitor conscious level, initial and progress every 15 minutes.
- For GCS less than 15, rule out hypoglycaemia, alcohol and drug overdose.
- Indication for endotracheal intubation.
- Life-threatening extracranial injuries e.g. hypotension and hypoxia always takes
priority over intracranial injuries.
- Non-life-threatening, time consuming procedures such as fracture fixation should
be postponed if possible.

2) Secondary survey
- Head injury: Scalp haematoma or laceration / CSF or blood from nose or ears /
Raccoon eyes / Battle sign / Sign of raised ICP (Cushings triad) / abnormal
respiratory pattern / Sign of herniation: pupillary dilatation.
- Examination of other systems.

3) Imagings
- Indications for skull radiograph.
- Indications for CT scanning.

4) Specific treatment
Scalp haematoma

Scalp laceration
Skull fracture

5) Upon assessment, decide either discharge, observe for 24 hours or transfer to

neurosurgical unit.

6) Cerebral protection
- Adequate oxygenation
- Hyperventilation:
- Release of hard collar.
- Head up position.
- IV Mannitol
- Analgesia and sedation.
- EVD.
- Decompressive craniectomy.

Appendix 1: Primary survey

Airway

Open up the airway: Head tilt-chin lift, empty the oral cavity, tongue
should not fall back, oropharyngeal (Guedel) tube if necessary.

Breathing

Look for chest expansion, percussion, auscultation. Identify the 6 lifethreatening chest conditions: Airway obstruction, Tension
pneumothorax, Massive haemothorax, Open pneumothorax, Flail chest
and Cardiac tamponade.

Circulation

Pulse (carotid), blood pressure, stop any bleeding, manage

haemorrhagic shock by large bore cannulae (x2), crystalloid infusion
and arrange for blood.

Disability

Conscious level (AVPU or GCS), pupil size and reaction. (AVPU: alert,
verbal stimuli response, painful stimuli response, unresponsive).

Exposure

Complete undress, warm blanket, maintain privacy.

Appendix 2: Glasgow coma scale (GCS)

Motor function
Obeying commands

Localizing

Flexion

Abnormal flexion

Extension

None

Verbal response
Oriented

Confused

Inappropriate words

Incomprehensible

None

Eye opening
Spontaneous

To speech

To pain

None

GCS 15 = M6V5E4

Appendix 3: Criteria for skull x-ray and CT scan

Criteria for skull radiograph

GCS of 14
History of LOC or amnesia

Persistent headache or vomiting

Scalp swelling or laceration
High impact injury

Criteria for CT scanning

Skull fracture on radiograph

Focal neurological deficit
Seizure
Battle sign (bruising over the mastoid)
Periorbital haematoma (raccoon or panda eye bruising)
Subconjunctival haemorrhage with no posterior limit
Blood or CSF in ears or nostrils
Difficult assessment in very young, very old or intoxication.