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Flashcards in Head injury Deck (27):

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

-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?


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 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
Neck pain


What signs are seen in SAH?

Neck stiffness
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?

Delayed ischaemic deficit
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


what is the presentation of an intracranial haemorrhage?


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