Hospital Based Practice – Head injury.

• Presentation varies from transient stunning for a few seconds, to prolonged coma.
• A fraction of patients who attend A&E with head injury need to be admitted for observation.
○ Admit patients who have.
 Confusion
 Abnormal CT
 Decreased GCS
 Clinical or radiological evidence of skull fracture.
 Neurological signs.
 Severe headache and vomiting
 Difficult assessment.
• Alcohol or drugs
• Very young or old
 Concurrent medical conditions.
• Eg. Clotting disorders
• Diabetes.
 Poor social circumstances/ lives alone.
○ If you do discharge a patient from A&E, they should be sent home with.
 A responsible adult who will remain with them for the next 24 hours.
 A head injury card that describes possible signs and symptoms.

• In the alert patient, assess the following.

○ Circumstances surrounding injury.
 Endogenous factors.
• Eg. Loss of conciousnes causing a fall
 Exogenous factors.
• Eg. Being knocked down.
 Any extracranial trauma.
○ Period of loss of consciousness
 Reflects severity of diffuse brain injury.
○ Period of post – traumatic amnesia.
 Period of antegrade amnesia reflects degree of brain damage
 Period of retrograde amnesia doesn’t accurately reflect severity of brain injury.
○ Headache or vomiting.
 Common after head injury.
 Persistant head injury and vomiting suggests raised ICP.
○ GCS
○ Any evidence of skull fracture.
○ Neurology.
 Any focal neurological signs.
○ Extracranial injury.
 Any evidence of occult blood loss.
• Drowsy or unconscious patient needs.
○ Urgent assistance from senior A&E and anaesthetic staff.
○ Protect airway.
 Intubate patients with deteriorating levels of consciousness
• Over breathing patient to induce hypocapnia can reduce ICP.
• This is controversial, consult an intensivist.
 Patients with no neurological deficit who are able to protect their airway don’t
require intubating.
 Assume there is a C – spine fracture until an X – ray has been performed that shows
all 7 cervical vertebrae are intact.
○ Hyperventilation.
 Note pattern of breathing.
• Central neurogenic respiration.
○ Regular, rapid deep and continuous breathings.
○ Rate of about 25 bpm.
○ No acidosis or hypoxia on blood gases.
○ Increasing regularity signifies progression of coma and worsening
prognosis
○ Due to diffuse damage to central areas of the brain.

• Apneustic breathing..
○ Prolonged inspiration, followed by period of apnoea.
○ Implies damage to pons.

• Cluster breathing.
○ Closely grouped respirations, followed by periods of apnoea.
○ Implies damage to pons.

• Ataxic breathing.
○ Chaotic and irregular mix of breathing and apnoea.
○ Implies damage to medullary respiratory centres.
○ Normally progresses to respiratory arrest quite quickly.
 • Biot’s respiration (gasping breathing)
○ Gasps for air, followed by apnoeic periods.
○ Implies damage to medullary respiratory centres.
○ Normally progresses to respiratory arrest quite quickly.

• Cheyne – Stoke respiration.

○ Periods of rapid, deep breathing followed by periods of apnoea.
○ Due to.
 Bilateral, deep hemisphere and basal ganglia damage.
 Cardiovascular dysfunction
 Respiratory dysfunction

• Slow, shallow breathing.

○ Due to medullary depression
○ Often due to opiates or benzodiazepine.
• Long tract signs.
○ Due to structural brainstem damage.
○ |Causes dysfunction of descending tracts.
○ Complex picture can occur due to decussation of pathways within
the brainstem.

○ Support circulation.
 Initially treat hypotension with colloids.
 If persistent or severe, exclude cardiac cause with ECG and occult haemorrhage (eg.
Intra abdominal).
○ Treat seizures
 Diazepam IV or PR.
 If continuing to fit give IV phenytoin.
○ Rapid survey of chest, abdomen and limbs.
 Flail chest
 Haemo/pneumothorax
 Intra abdominal bleeding
 Limb lacerations
 Long bone fractures.
○ Brief history.
 Obtain from ambulance crew or relatives.
 Establish if patient lost consciousness before or after the head injury.
• Faints or SAH can cause loss of consciousness, and so cause a fall and head
injury, rather than the head injury causing the loss of consciousness.
○ Gain a feel for the tempo of neurological deterioration.
• Symptoms of minor head injury.
○ Headache
○ Dizzines
○ Fatigue
○ Reduced concentration
○ Memory deficit
○ Irritability
○ Anxiety
○ Insomnia
○ Hyperacusis
○ Photophobia
○ Depression
○ Generally slowed information processing.

• Symptoms of a major head injury.

○ Any symptoms of minor head injury.
○ Behavioural problems.
 Irritability
 Impulsivity
 Egocentricity
 Emotional lability
 Impaired judgement
 Impatience
 Anxiety
 Depression
 Hyper or hyposexuality
 Dependency
 Euphoria
 Aggressiveness
 Apathy
 |Childishness
 Disinhibition.
○ Cognitive impairment.
 Memory deficits
 Difficulty in abstract thinking
 Generally slowed information processing.
 Poor concentration
 Slowed reaction time
 Impaired auditory comprehension
 Reduced verbal fluency
 Anomia
  Difficulty planning or organising.

• Examination.
○ Rapid neurological examination should only take a few minutes.
 GCS
 Pupil.
• Size
• Shape
• Reaction to light
 Resting eye position.
 Spontaneous eye movements.
• If reduced and patient unresponsive, look for oculocephalic and
oculovestibular reflexes.
○
• Don’t do Doll’s head manoeuvre until C – spine fracture has been exclude.
 Assess motor function.
• Note any asymmetry.
 Look for features suggesting brain shift or herniation.
○ Head and spine assessment.
 Examine skull for fractures
• 1% will have fractures.
• Fracture increases the risk of intercranial haematoma from
○ 1:1000 to 1:30 in alert patients.
○ 1:00 to 1:4 in confused or comatose patients.
• Absence of skull fracture does not rule out potentially fatal injuries.
 Basal skull fractures are suggested by.
• Extensive periorbital haematoma
• Bruising behind the ear.
○ Battle’s sign.
• Bleeding from the ear.
• Leaking of CSF from nose or ear.
 Check for facial fractures
• Maxillary
• Mandibular.
 Consider possibility of spinal cord trauma.
• Log roll patient.
• Examine for.
○ Tenderness over spinous processes
○ Paraspinal swelling
○ Gap between spinous processes
○ Flaccid and anaesthetised limbs
 ○ Painless urinary retention.

• Investigations.
○ Indications for skull x – ray.
 History of high – impact injury
 Decreased level of consciousness
 Amnesia
 Nausea or vomiting
 Neurological signs or symptoms
 CSF/ blood from nose/ear
 Scalp bruising or swelling
 Suspected penetrating injury
 Difficulty in clinical assessment.
• Elderly
• Young
• Alcohol
• Drugs
 Seizures
○ Things to look for on skull x – ray.
 Linear skull fractures
 Depressed skull fracture.
• Requires elevation if depressed by more than the thickness of the vault.
 > 3 mm shift of a calcified pineal (if present).
 Integrity of craniocervical junction.
 Fluid level in sphenoid sinus.
○ Things to look for on C – spine film.
 Check all 7 cervical vertebrae.
 Check integrity of C7 – T1 junction.
 Check alignment.
• Anterior and posterior vertebral bodies
• Posterior margin of spinal canal
• Spinous processes

• Step of 25% of vertebral body suggests facet joint dislocation.

 Check contours.
• Outlines of vertebral bodies
• Outlines of spinous processes

• Avulsion fractures
• Wedge fractures
○ Difference of > 3 mm between anterior and posterior body heights.
 Check odontoid.
 • Should be < 3 mm between anterior arch of C1 and odontoid.
 Disc spaces.
• Space > 5 mm between anterior C3 and back pharyngeal shadow suggests
retropharyngeal mass.
• Abscess
• Haematoma from fracture of C2.

○ Indications for urgent CT.

 GCS < 12
 Skull fracture and persistent neurological dysfunction
 Neurological dysfunction, eg. Seizures.
 Coma after resuscitation
 Suspected compound fracture of vault or base of skull, eg. CSF leak.
 Persistent confusion of neurological disturbances at 12 hours.
 Significant head injury requiring general anaesthesia.
○ Indication for neurosurgical referral.
 Recent intracranial lesion seen on CT
 Persisting coma after initial resuscitation
 Confusion the persists at 4 hours.
 Progressive focal neurological signs
 Seizure without full recovery
 Depressed skull fracture
 Suspected penetrating injury
 Signs of basal skull fracture
 Need for urgent CT, but facilities not available.

• Management.
○ Resuscitate.
○ Take bloods for.
 FBC
 U&E
 Group & Save
 ABGs
 Toxicology screen.
• If appropriate.
○ Subsequent management depends on pace of development.
 40% of comatose head injury patients have intracranial haemorrhage.
 Not possible to distinguish clinically between diffuse brain injury and intracranial
haemorrhage.
○ CT scan.
 Most patients who need resuscitation will need CT.
 Urgency depends on rate of deterioration.
○ Treat raised ICP.
 If present.
 Very severe injuries may require simultaneous surgical decompression and
resuscitation.
 May need to reduce ICP while waiting for CT scan.
• Mannitol
 • Hyperventialtion to cause hypocapnia
• Frusemide.

○ Surgery.
 May be indicated for.
• Extradural haemorrhage
• Subdural haemorrhage
• Intracranial haemorrhage.
○ Rarely.
• Complex head wounds.
○ Eg. Compound depressed skull fractures.
 Generally, urgent evacuation is required if an extradural haematoma.
• Causes midline shift of > 5 mm
• Volume of > 25 ml.
 If haematoma too small to evacuate on original CT scan, rescan at 9 – 12 hours
regardless of any improvement or deterioration of condition.
○ Non – operative management.
 Brain contusions may be seen as areas of low density on CT.
 CT is a very poor way of detecting primary diffuse brain injury.
 Raised ICP may be seen as effacement of
• Cavity of 3rd ventricle
• Perimesencephalic cisterns.
• Further management.
○ Aim is to reduce and minimise secondary brain injury.
 Causes of secondary brain injury.
• Systemic
○ Hypoxaemia
○ Hypotension
○ Hypercarbia
○ Severe hypocapnoea
○ Pyrexia
○ Hyponatraemia
○ Anaemia
○ DIC
• Intracranial.
○ Haematoma.
 Extradural
 Subdural
 Intracerebral.
○ Brain swelling/ oedema
○ Raised ICP
○ Cerebral vasospasm
 ○ Epilepsy
○ Intracranial infection.
○ Management may be better undertaken at a neurosurgical centre.

○ Principles of management are.

 Regular monitoring.
• If there is deterioration, consider a secondary brain injury.
• Intubate if.
○ New signs of raised ICP
○ Declining levels of consciousness
○ Signs of transtentorial herniation

○ Consider over – breathing and mannitol

 Close monitoring of BP, ABG, electrolytes and urine output.
• Pre – emptive treatment may prevent neurological decline.
• Hypotension is common due to.
○ Sedatives
○ Hypovolaemia
 Replace fluids carefully so as to not aggravate raised ICP.
 Prompt treatment of seizure.
 Insert NG tube.
• Nutrition
• Drugs.
○ Ranitidine for peptic ulcer prophylaxis.
 Stool softeners.
• Straining can aggravate raised ICP.

○ Before transfer to Neurosurgical unit.

 Assess for.
• Respiratory insufficiency
• Shock
• Internal injury.
 Perform.
• CXR
• ABG
• C – spine X – ray
 Consider appropriate treatment, which may include.
• Intubation
○ If airway threatened or obstructed.
• Ventilate.
○ Cyanosis
○ PaCO2 > 5.9 kPa
 ○ PaO2 < 7.9 kPa
• IV fluids.
○ Commence carefully.
• Mannitol
○ Discuss with neurosurgeon first
• Cervical collar or traction.
 Transfer with staff who are able to intubate, ventilate, cannulate and suction.