Neurology - Head injury and GCS Flashcards
2 types of head injury
Missile and non-missile injuries (more common)
What is a missile injury? Name the 3 types of injury
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
What are non-missile brain injury?
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)
Primary brain damage
Consequence of non-missile brain damage
= Damage that occurs at the time of injury in 2 main forms: focal damage and diffuse axonal injury
Focal damage
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)
What do healed contusions look like?
Wedge shaped areas of gliosis that are yellow/brown due to the presence of haemosiderin
Diffuse axonal injury
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
What are the 2 main components of diffuse axonal injury?
- ) Small haemorrhagic lesions in the white matter of corpus callosum and brainstem
- ) 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
Secondary brain damage
Results from complications developing after the moment of injury
- ) Intracranial haemorrhage - various types
- ) Traumatic damage to extra-cerebral arteries - uncommon but important, e.g. direction of internal carotid
- ) Cerebral oedema - raised ICP leading to herniation
- ) Hypoxic brain damage - hypotension following blood loss, raised ICP (rarer causes include fat emboli and trauma to extra cerebral vessels)
- ) Meningitis - esp open skull fracture
Extradural haematoma
= 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
Subdural haematoma
= 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
Intracerebral/ intraparenchymal haemorrhage
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
What are the risk factors/ associations for TBI?
- 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
High risk groups for TBI
- 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
Immediate management of head injury
- ABC approach
- Spinal immobilisation (spinal injuries are strongly associated with head injury)
- Establish GCS score
Important points in the history of TBI
(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
What is post traumatic amnesia (PTA)?
= 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
Examination of a patient with TBI
- ) Evidence of injury - lacerations, grazing, bruising (be careful! - traumatic intracranial haematoma can occur in patients with no evidence of trauma)
- ) Basal fracture signs
- ) Conscious level - GCS
- ) Pupil response
- ) Limb weakness
- ) Eye movements
What are the features of a base of skull fracture?
Anterior fossa fracture:
1.) CSF rhinorrhoea - if nasal discharge contains glucose then the fluid is CSF rather than mucin
- ) Bilateral periorbital bruising - indicates blood tracking from behind
- ) 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”
Components of GCS
- 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
How is pupillary response tested in TBI?
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
How can a IIIrd nerve lesion be an important localising sign in head injury?
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)
How can limb weakness be assessed in an unconscious patient?
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
On which side does hemiparesis/ hemiplegia usually occur following head injury? What is Kernohan’s notch?
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
