Head injury Flashcards
What is primary brain injury?
This is when sudden acceleration, deceleration or rotation causes the brain to move so much in the skull that causes:
Tearing of nerve fibres Petechial haemorrhages within the white matter Contusions and lacerations of the cortex
Secondary brain injury is when the initial head injury causes the brain to be diffusely damaged and therefore vulnerable to 4 other insults - what are these?
-what do all four of these cause?
Arterial hypotension:
- From blood loss at the time of injury: scalp/elsewhere in body
- Hypotension and/or hypoxia can cause hypoxic-ischaemic brain damage with swelling
Arterial hypoxia:
-Due to airway obstruction/assoc. chest injury/epileptic fit
Infection:
- Head injuries by which skull fracture has occurred can allow organisms to enter the skull
- Infection causes inflammatory oedema
Intracranial haematoma:
-Force of injury may have torn a vessel inside the skull = haematoma
-Either in brain substance or meninges
= compression
These all cause further brain swelling and encourage downward cascade to brainstem failure and death
describe the pathophysiology of primary brain injury and how this can allow secondary brain injury
The release of excitatory amino-acids (glutamate/aspartate) bind to receptors (e.g.NMDA)
This causes the release of intracellular calcium and the activation of phospholipases This leads to the breakdown of cell membranes, cell swelling and activation of apoptosis
This leads to secondary brain injury from:
Loss of blood-brain-barrier Leucocyte infiltration = inflammation Loss of cerebral autoregulation of blood pressure = ischaemia Loss of cerebral autoregulation of blood flow = metabolic decoupling = even more ischaemia causing further brain oedema
What is cerebral perfusion pressure? what CPP is aimed for after brain injury?
CPP = MAP - ICP
Hypotension has a major influence on CPP Aim for CPP of > 60mmHg after head injury ie MAP > 80mmHg and keeping ICP < 20mmHg Normal adult ICP is 9-11mmHg (12 -15 cm H2O)
What clinical features are seen in a skull base fracture?
haematoma over mastoid (battle sign) – middle cranial fossa
bilateral periorbital haematoma (panda eyes) – anterior cranial fossa Subconjuctiva haematoma – blood under conjunctiva with no posterior margin indicating blood tracking forward from orbit CSF discharge from nose or ear (clear fluid) Bleedng from ear
When should a CT head be performed immediately after a brain injury?
GCS < 13 on initial assessment
GCS < 15 at 2 hours post-injury
suspected open or depressed skull fracture.
any sign of basal skull fracture (haemotympanum, ‘panda’ eyes, cerebrospinal fluid leakage from the ear or nose, Battle’s sign).
post-traumatic seizure.
focal neurological deficit.
more than 1 episode of vomiting
Taking anti-coagulants
When should a CT scan be perfomed within 8 hours of injury?
for adults with any of the following risk factors who have experienced some loss of consciousness or amnesia since the injury:
- age 65 years or older
- any history of bleeding or clotting disorders
- dangerous mechanism of injury (a pedestrian or cyclist struck by a motor vehicle, an occupant ejected from a motor vehicle or a fall from a height of greater than 1 metre or 5 stairs)
- more than 30 minutes’ retrograde amnesia of events immediately before the head injury
What methods of cerebral protection exist following brain injury?
CSF Drainage-reduces ICP
Mannitol -improves micro-perfusion
Hypertonic saline-may be better than mannitol
Hyperventilation-temporary effect (2-4 hrs)
Hypothermia -weak evidence for effect
Decompressive craniectomy – randomised trial underway
Describe the mechanism of injury and clinical features of an extradural haematoma?
Bleeding into the space between the dura mater and the skull. Often results from acceleration-deceleration trauma or a blow to the side of the head. The majority of epidural haematomas occur in the temporal region where skull fractures cause a rupture of the middle meningeal artery.
Features
features of raised intracranial pressure some patients may exhibit a lucid interval
What does an extradural haematoma look like on CT?
Convex shaped - skulls sutures where dura mater is attached to the skull constricts the haematoma
Describe the mechanism of injury and clinical features of a subdural haematoma?
Bleeding into the outermost meningeal layer. Most commonly occur around the frontal and parietal lobes.
due to stretching and tearing of bridging cortical veins as they cross the subdural space to drain into an adjacent dural sinus.
Risk factors include old age, alcoholism and anticoagulation.
Slower onset of symptoms than a epidural haematoma.
Describe the appearance of subdural haematoma on CT?
lens shaped
What is the mechanisms of injury and clinical features of a subarachnoid haemorrhage?
Usually occurs spontaneously in the context of a ruptured cerebral aneurysm but may be seen in association with other injuries when a patient has sustained a traumatic brain injury
What is the cushings reflex and is this an early or late sign of brain injury?
the Cushings reflex (hypertension and bradycardia) often occurs late and is usually a pre terminal event
SAH - what is the presentation
Sudden onset severe headache Collapse Vomiting Neck pain Photophobia
What signs are seen in SAH?
Neck stiffness
Photophobia
Decreased conscious level
Focal neurological deficit (dysphasia, hemiparesis, IIIrd n. palsy)
Fundoscopy - retinal or vitreous haemorrhage
What is the role of lumbar puncture in SAH?
Safe in alert patient with no focal neurological deficit and no papilloedema, or after normal CT scan
bloodstained or xanthochromic CSF (6-48hr)
differentiate from ‘traumatic tap’
What is the gold standard test for SAH?
Cerebral angiography:
Seldinger technique via femoral artery
Digital Subtraction
4 vessel angiography with multiple views
Gold standard but occ. may miss an aneurysm due to vasospasm
Magnetic resonance and CT techniques increasingly used
What are the complications of SAH?
Re-bleeding Delayed ischaemic deficit Hydrocephalus Hyponatraemia Seizures - give anticonvulsant prophylaxis
Rebleeding in SAH - how is this prevented?
Often fatal 20% risk in first 14 days 50% risk in first 6 months Endovascular techniques Surgical clipping
What is delayed ischaemia in SAH?
Delayed ischaemic Neurological Deficit (DIND)
Days 3-12
altered conscious level or focal deficit
Vasospasm - Nimodipine can be used to prevent this
To prevent: High fluid intake due to Triple H therapy
Hydrocephalus in SAH: what is the clinical features and treatment?
Increased intracranial CSF pressure
6% symptomatic
Increasing headache or altered conscious level
Often transient
Treatment - CSF drainage - LP, EVD, Shunt
Why does SAH cause hyponatraemia? what is the treatment?
SIADH or ‘cerebral salt wasting’ Often transient Do not fluid restrict supplement sodium intake fludrocortisone
what is the presentation of an intracranial haemorrhage?
Headache
Focal neurological deficit
Decreased conscious level
what are the investigations of an intracranial haemorrhage?
CT scan - urgent if decreased conscious level
Angiography if suspicion of underlying vascular anomaly
What is the treatment of ICH?
Surgical evacuation of haematoma +/-treatment of underlying abnormality
Non-surgical management
What is an intraventricular haemorrhage?
Occurs with rupture of a subarachnoid or intracerebral bleed into a ventricle
Any combination of subarachnoid, intracerebral and intraventricular haemorrhage can occur
