Head injury Flashcards

1
Q

What is primary brain injury?

A

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
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2
Q

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?

A

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

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3
Q

describe the pathophysiology of primary brain injury and how this can allow secondary brain injury

A

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
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4
Q

What is cerebral perfusion pressure? what CPP is aimed for after brain injury?

A

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)
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5
Q

What clinical features are seen in a skull base fracture?

A

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
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6
Q

When should a CT head be performed immediately after a brain injury?

A

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

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7
Q

When should a CT scan be perfomed within 8 hours of injury?

A

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
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8
Q

What methods of cerebral protection exist following brain injury?

A

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

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9
Q

Describe the mechanism of injury and clinical features of an extradural haematoma?

A

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
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10
Q

What does an extradural haematoma look like on CT?

A

Convex shaped - skulls sutures where dura mater is attached to the skull constricts the haematoma

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11
Q

Describe the mechanism of injury and clinical features of a subdural haematoma?

A

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.

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12
Q

Describe the appearance of subdural haematoma on CT?

A

lens shaped

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13
Q

What is the mechanisms of injury and clinical features of a subarachnoid haemorrhage?

A

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

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14
Q

What is the cushings reflex and is this an early or late sign of brain injury?

A

the Cushings reflex (hypertension and bradycardia) often occurs late and is usually a pre terminal event

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15
Q

SAH - what is the presentation

A
Sudden onset severe headache
Collapse
Vomiting
Neck pain
Photophobia
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16
Q

What signs are seen in SAH?

A

Neck stiffness
Photophobia
Decreased conscious level
Focal neurological deficit (dysphasia, hemiparesis, IIIrd n. palsy)
Fundoscopy - retinal or vitreous haemorrhage

17
Q

What is the role of lumbar puncture in SAH?

A

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’

18
Q

What is the gold standard test for SAH?

A

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

19
Q

What are the complications of SAH?

A
Re-bleeding
Delayed ischaemic deficit
Hydrocephalus
Hyponatraemia
Seizures - give anticonvulsant prophylaxis
20
Q

Rebleeding in SAH - how is this prevented?

A
Often fatal
20% risk in first 14 days
50% risk in first 6 months
Endovascular techniques
Surgical clipping
21
Q

What is delayed ischaemia in SAH?

A

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

22
Q

Hydrocephalus in SAH: what is the clinical features and treatment?

A

Increased intracranial CSF pressure
6% symptomatic
Increasing headache or altered conscious level
Often transient
Treatment - CSF drainage - LP, EVD, Shunt

23
Q

Why does SAH cause hyponatraemia? what is the treatment?

A
SIADH or ‘cerebral salt wasting’
Often transient
Do not fluid restrict
supplement sodium intake
fludrocortisone
24
Q

what is the presentation of an intracranial haemorrhage?

A

Headache

Focal neurological deficit

Decreased conscious level

25
Q

what are the investigations of an intracranial haemorrhage?

A

CT scan - urgent if decreased conscious level

Angiography if suspicion of underlying vascular anomaly

26
Q

What is the treatment of ICH?

A

Surgical evacuation of haematoma +/-treatment of underlying abnormality

Non-surgical management

27
Q

What is an intraventricular haemorrhage?

A

Occurs with rupture of a subarachnoid or intracerebral bleed into a ventricle

Any combination of subarachnoid, intracerebral and intraventricular haemorrhage can occur