Neurology - Head injury and GCS

Question 1

2 types of head injury

Answer 1

Missile and non-missile injuries (more common)

Question 2

What is a missile injury? Name the 3 types of injury

Answer 2

Caused by bullets or small objects propelled through the air.

3 main types of injury:
1) Depressed = missile causes depressed skull fracture but does not enter the brain

2) Penetrating injuries = object enters the cranial cavity but does not exit. Focal neurology often accompanied by infection
3) Perforating injuries = missile enters AND exits from the cranial cavity leaving an exit wound. Brain damage around the missile tract is usually severe

Question 3

What are non-missile brain injury?

Answer 3

Range from relatively minor injuries with spontaneous improvement (e.g. concussion) to severe injuries that a rapidly fatal

Occur most commonly in RTAs (55%) and falls (35%) - rotational forces + impact related forces that often cause skull fracture (although not always)

Question 4

Primary brain damage

Answer 4

Consequence of non-missile brain damage

= Damage that occurs at the time of injury in 2 main forms: focal damage and diffuse axonal injury

Question 5

Focal damage

Answer 5

E.g. contusions (most common form of focal damage)
These usually occur at the impact site especially if skull fracture is present

They are asymmetrical - often occur on the side opposite the impact = “Countrecoup lesions”

After injury the brain comes into contact with adjacent bone causing local injury (i.e. cranial nerve lesion or brainstem damage)

Large contusions often produce haemorrhage and haematomas (collection of blood)

Question 6

What do healed contusions look like?

Answer 6

Wedge shaped areas of gliosis that are yellow/brown due to the presence of haemosiderin

Question 7

Diffuse axonal injury

Answer 7

Occurs as a result of shearing and tensile forces produced by rotational movements of the brain within the skull

Often occurs in the absence of skull fractures or cerebral contusions

Question 8

What are the 2 main components of diffuse axonal injury?

Answer 8

1. ) Small haemorrhagic lesions in the white matter of corpus callosum and brainstem
2. ) Diffuse damage to axons - this can only be detected microscopically in the form of axonal beads and swelling in the white matter. Damaged axons eventually degenerate - loss of white matter fibres

Question 9

Secondary brain damage

Answer 9

Results from complications developing after the moment of injury

1. ) Intracranial haemorrhage - various types
2. ) Traumatic damage to extra-cerebral arteries - uncommon but important, e.g. direction of internal carotid
3. ) Cerebral oedema - raised ICP leading to herniation
4. ) Hypoxic brain damage - hypotension following blood loss, raised ICP (rarer causes include fat emboli and trauma to extra cerebral vessels)
5. ) Meningitis - esp open skull fracture

Question 10

Extradural haematoma

Answer 10

= Bleed between the dura and the skull

Cause = skull fracture with arterial rupture - classically it is the middle meningeal artery

Clinical - lucid interval followed by rapid increase in ICP as haemorrhage strips dura from bone

Question 11

Subdural haematoma

Answer 11

= Bleed between the dura and arachnoid mater

Cause = rupture of venous sinus or small bridging veins due to torsion forces

Clinical - acute presentation with rapid increase in ICP
- chronic presentation with personality change, memory loss and confusion especially in the elderly

Question 12

Intracerebral/ intraparenchymal haemorrhage

Answer 12

Cause = cortical contusions, or rupture of small intrinsic vessels within intracerebral haematoma or “burst lobe” (= intracerebral + subdural in temporal lobe)

Clinical - depends on the degree of bleed, can cause seizures or increased ICP with focal deficits

Question 13

What are the risk factors/ associations for TBI?

Answer 13

• Alcohol intoxication - 40%
• Patients on anticoagulation or anti platelet therapy, or with known bleeding diatheses are at increased risk of intracranial haemorrhage following TBI
• Children with ADHD
• Low SES

Question 14

High risk groups for TBI

Answer 14

• Young children (0-4 years)
• Young adults (15-19 years)
• Elderly (>75 years)

NB - males are twice as likely as females to sustain a TBI

Question 15

Immediate management of head injury

Answer 15

• ABC approach
• Spinal immobilisation (spinal injuries are strongly associated with head injury)
• Establish GCS score

Question 16

Important points in the history of TBI

Answer 16

(May have to gain collateral)

• Mechanism of injury
• Timing of accident
• Duration of LOC
• Associated injuries - e.g. headache and vomiting may indicate raised ICP
• Occurrence of a “lucid interval” suggesting secondary complication

Question 17

What is post traumatic amnesia (PTA)?

Answer 17

= transient state of altered consciousness and behaviour following concussive type injuries

Characteristic deficiencies are (i) anterograde amnesia (inability to form new memories following TBI) and (ii) disorientation

Reflects severity of brain damage

Question 18

Examination of a patient with TBI

Answer 18

1. ) Evidence of injury - lacerations, grazing, bruising (be careful! - traumatic intracranial haematoma can occur in patients with no evidence of trauma)
2. ) Basal fracture signs
3. ) Conscious level - GCS
4. ) Pupil response
5. ) Limb weakness
6. ) Eye movements

Question 19

What are the features of a base of skull fracture?

Answer 19

Anterior fossa fracture:
1.) CSF rhinorrhoea - if nasal discharge contains glucose then the fluid is CSF rather than mucin

2. ) Bilateral periorbital bruising - indicates blood tracking from behind
3. ) Subconjunctival haemorrhage - bruising under the conjunctiva extending to the limits of the sclera indicates blood tracking from orbital cavity

Petrous fracture:
- Bleeding from external auditory meatus - look for “Battle’s sign”

Question 20

Components of GCS

Answer 20

• Eye opening (4)
• Best verbal response (5)
• Best motor response (6)

NB - none of these components can be scored 0, so GCS 3 is the lowest score

Question 21

How is pupillary response tested in TBI?

Answer 21

Light reflex tests both CNII and CNIII but CNIII is the most useful indicator of an expanding intracranial lesions

Herniation of the medial temporal lobe through the tentorial hiatus may damage the IIIrd nerve either:

i) Directly - by compression
ii) Indirectly - causes midbrain ischaemia resulting in pupil dilation with impaired or absent light reflex

Question 22

How can a IIIrd nerve lesion be an important localising sign in head injury?

Answer 22

IIIrd nerve lesions cause the pupil to become dilated (because of interrupted parasympathetic supply to the eye) with impaired or absent response to light (IIIrd nerve carries efferent impulse in the light response)

= pupil dilates on the side of the expanding lesion (e.g. haematoma, oedema)

Question 23

How can limb weakness be assessed in an unconscious patient?

Answer 23

Limb weakness can be detected by localisation to pain

If pain produces an asymmetric response - i.e. both arms do different things such as flexion, extension or one arm “localising” then limb weakness is present

NB - flexion to pain is associated with low GCS

Question 24

On which side does hemiparesis/ hemiplegia usually occur following head injury? What is Kernohan’s notch?

Answer 24

Usually occurs in the limbs contralateral to the side of the lesion

Indentation of the contralateral cerebral peduncle by the edge of the tentorium cerebelli (Kernohan’s notch) may produce an ipsilateral deficit - this is a FALSE localising sign most often seen with chronic subdural haematoma

Question 25

What are the 2 reflex eye movements that can be tested for in an unconscious patient?

Answer 25

i) Oculocephalic (Doll’s eye) reflex
ii) Oculovestibular reflex (caloric stimulation)

Abnormal eye movements may result from: brain stem dysfunction, damage to nerves supplying extra ocular muscles or damage to vestibular apparatus

Question 26

NICE guidelines for imaging in TBI

Answer 26

CT head is the investigation of choice - request immediately if any of the following are present:
- GCS

Question 27

When can the CT head be delayed following TBI?

Answer 27

It isn’t always necessary to get a CT head immediately, it can wait up to 8 hours after injury in certain circumstances:

• Age > 65 years
• Dangerous mechanism of injury (e.g. pedestrian or cyclist struck by a motor vehicle)

Question 28

Below what GCS score do patients with severe head injury require intubation?

Answer 28

Patients with a GCS less than or equal to 8 require intubation and ventilation

They should also have ICP monitoring to allow early detection of any raise in ICP

In severe head injury the aim is to maintain cerebral perfusion pressure between 60-70mmHg

Question 29

Intoxication and depressed GCS

Answer 29

It is important to exclude significant brain injury before ascribing reduced GCS to intoxication

Alcohol intoxication is unlikely to account for a loss of more than one GCS point (even with severe intoxication or blood alcohol of >250mg/dL) - don’t wait, get a scan!

Question 30

Principle of TBI management

Answer 30

The key in TBI management involves prevention of secondary insults to the damaged brain - these can be (i) systemic or (ii) intracranial (raised ICP being the most important)

Question 31

How are hypoxia, hypercapnia, anaemia and hyponatraemia managed following TBI?

Answer 31

All examples of systemic complications along with sepsis, hypotension, hyper or hypoglycaemia, and pyrexia

Hypoxia:

• Ensure patent airway and optimise ventilation/ ventilate
• Maintain PaO2 > 10kPA

Hypercapnia:
- Ensure patent airway, ventilate if GCS 10g/dL; transfuse if required

Hyponatraemia:
- Maintain Na+ > 140mmol/L using saline or mannitol; do not correct too rapidly (risk central pontine myelinolysis)

Question 32

How long is phenytoin given following TBI?

Answer 32

Prophylactic phenytoin is given for 7 days to prevent early seizures; anticonvulsants are continued if seizures occur

Question 33

List some complications of TBI?

Answer 33

1) Epilepsy - risk is highest in first 3 years after injury; higher risk with penetrating (missile) injuries
2) CSF leak/ meningitis - CSF otorrhoea almost always resolves spontaneously; nasal CSF persisting for > 7 days may require intervention
3) Hydrocephalus - may develop months - years after; normal pressure symptoms common
4) Brain abscess (especially with penetrating)
5) Post concussion symptoms - e.g. headache, dizziness, memory problems
6) Hypopituitarism - up to 15% of patients with severe injury; diabetes insipidius may occur to posterior pituitary failure
7) Dementia pugilistica - dementia related to repeated head injury

Question 34

What determines prognosis in TBI?

Answer 34

3 severities - mild, moderate and severe:

• Mild 98%
• Moderate 85%
• Severe 50%

Determined by:

(i) Admission GCS (motor score most reliable)
(ii) Duration of PTA
(iii) Duration of LOC

Question 35

Important differentials to consider in TBI

Answer 35

• Coma
• Subarachnoid haemorrhage; if not definite history of trauma or if symptoms precede traumatic event (i.e. headache then fall)
• High cervical cord injury; beware as a cause of absent motor responses when assessing GCS