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Session 3: skull base & head > Station 4: head injury > Flashcards

Station 4: head injury Flashcards

1
Q

What is the usual cause of death in severe head injuries with a variable period of survival?

A

Raised intracranial pressure - as a result of either brain swelling or of a haemorrhage accumulating inside the skull.

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2
Q

What is the most usual neuropathological cause of long-term disability after a head injury?

A

Damage to axons and hypoxic-ischaemic damage, sustained at time of injury.

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3
Q

What are the two important mechanisms involved in head injury?

A

Impact to the head and movement of the brain.

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4
Q

What are the two most useful ways to classify head injury?

A

Focal or diffuse

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5
Q

What does the term focal indicate in head injury?

A

Pathology that can be seen on CT or MRI - which may be neurosurgically treatable.

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6
Q

What does the term diffuse indicate in head injury?

A

Microscopic damage which cannot be demonstrated by any of the current imaging techniques, clinicians diagnose this when they have an unconscious patient whose scan shows very little obvious damage.

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7
Q

What types of skull fracture are there?

A

Depressed, comminuted, linear

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8
Q

What type of skull fracture is most likely to occur from a RTA involving a motorcyclist wearing a helmet?

A

Linear fracture

Helmet dissipates force

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9
Q

How does papilloedema develop in head injury?

A

Optic disc swelling

A raised intracranial pressure following head trauma can cause bilateral optic disc swelling.
The optic nerve sheath is continuous with the subarachnoid space, the increased ICP is transmitted to the subarachnoid space surrounding the optic nerve. The pressure prevents axonal flow back along the nerve, causing swelling and protrusion of the optic nerve at its head into the globe. Ultimately compressing the optic nerve and impeding its venous return.

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10
Q

What is visible papilloedema?

A

Retinal veins that produce capillary leak around optic disk

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11
Q

What is the Cushing’s reflex and how does it develop in head injury?

A

Trauma -> raised ICP -> compression of blood vessels supplying the brain -> reduced blood flow to the brain resulting in ischaemia -> sympathethic peripheral vasoconstriction and increased cardiac output -> increase arterial BP -> increase perfusion of the brain (to perfuse the brain, arterial blood pressure = MAP must be greater than that of intracranial pressure so CPP = MAP - ICP) -> baroreceptors in carotid bodies -> bradycardia

Triad: hypertension, bradycardia and irregular respirations in a patient with increased ICP

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12
Q

What is the battle sign that you can develop in head injury?

A

Mastoid ecchymosis
Middle cranial fossa basilar skull fracture (base of skull fracture) - fractures of petrous temporal bone
Periosteal bleeding, draining towards exterior from basilar fracture, develops for several hours following trauma

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13
Q

How does a facial nerve palsy develop following head trauma?

A

The facial nerve runs through the temporal bone.
Skull fracture across temporal bone (basilar fracture) or shearing contents in middle ear -> facial nerve contusion/transection leading to paralysis hours or days post trauma.

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14
Q

What is an indication in head trauma to test the facial nerve?

A

Haemotympanum (blood seen in the tymanic cavity of the middle ear) indicating a base of skull fracture

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15
Q

What are common features of an anterior cranial fossa fracture?

A

CSF rhinorrhoea

Racoon eyes

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16
Q

What are the common features of middle cranial fossa fracture?

A

CSF otorrhoea
Haemotympanum
Battle sign
Facial nerve palsy (CNVII)

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17
Q

What are the common features of a posterior cranial fossa fracture?

A

Bruising over suboccipital area

Cranial nerve injuries

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18
Q

What are the possible causes of ‘mass effect’ in the brain?

A

Space occupying lesion: trauma, haematoma, tumour, cerebral oedema

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19
Q

What is the Monro-Kellie hypothesis?

A

Pressure-volume relationship, aiming to keep a dynamic equilibrium among essential non-compressible components inside the rigid compartments of the skull.

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20
Q

What is the average intracranial volume of an adult and what is it composed of?

A 
Average volume around 1700ml.
Composed of:
Brain tissue (1400ml)
CSF (150ml)
Blood (150ml)

The volume of each remains nearly constant in a state of dynamic equilibrium so a decrease in one should be compensated by an increase in another.

21
Q

What is the main protection to the brain when the intracranial volume increases?

A

Blood and CSF

22
Q

What happens when there is intracranial pathology?

A

The volume of one component within the cranium increases e.g. heamatoma, brain swelling. When the initial compensatory mechanisms are exhausted (which tries to prevent major changes in the ICP), there is a marked increase in ICP -> reduction CPP -> cerebral ischaemia

23
Q

Explain the phases of the ICP-volume compliance curve

A

Beginning of curve (A+B):
Compensation phase -> ICP nearly constant with an increase in intracranial volume initially

Steep curve (C+D):
Decompensation phase -> ICP increase rapidly with increase ICV as buffers exhausted.
24
Q

What system is the blood in the cranial cavity mostly contained in?

A

Low pressure venous system - venous compression serves as a means of displacing blood volume

25
Q

What happens as a result of a rapidly increase ICP?

A

Herniation

26
Q

What are the later signs of raised ICP?

A 
Loss of consciousness (reduced GCS)
Cushing's triad
Pupil asymmetry/dilatation
Projective vomiting
Hemiplegia/decorticate/decerebrate
27
Q

What is subfalcine herniation?

A

Displacement of brain (typically cingulate gyrus) beneath free edge of falx cerebri due to raised intracranial pressure –>
diffuse hemispheric oedema, compressed/flattened gyri on affected side and midline shift

28
Q

What is tentorial/uncal herniation?

A

Transtentorial herniation has two subtypes:

  1. Uncal = descending
  2. Ascending transtentorial

The uncus and adjacent part of temporal lobe glide downwards across tentorial notch compressing brainstem and posterior cerebral arteries in the ambient cistern.

29
Q

What is tonsillar herniation?

A

Inferior descent of the cerebellar tonsils below the foramen magnum.
Tonsil compresses on the dorsal part of medulla which can be fatal as it can affect the cardiac and respiratory centres if left untreated.

30
Q

What effects does herniation have on the brain?

A
  • Distorting and causing pressure on the brain
  • Compresses blood vessels leading to secondary ischaemic damage
  • Cranial nerves can be compressed
31
Q

Which type of herniation is the most common?

A

Subfalcine herniation

32
Q

Which artery can be occluded in cases of subfalcine herniation? What are the likely symptoms?

A

Anterior cerebral artery infarct - clinical symptom of contralateral leg weakness

33
Q

What is the triad of features which constitute the Cushing reflex (vasopressor response) as seen in raised ICP? What is it a late sign of?

A
  1. Hypertension
  2. Bradycardia
  3. Irregular respiration (impaired brainstem function)

Terminal stages of acute head injury - may indicate imminent herniation.

34
Q

What are the components of uncal herniation?

A

Oculomotor (CNIII)
PS input to affected eye -> pupil dilates, fails to constrict in response to light
Somatic motor -> down and out only CNIV and CNVI working

Compress ipsilateral posterior cerebral artery

  • ipsilateral primary visual cortex
  • contralateral homonymous hemianopia

Compress contralateral cerebral crus
(corticospinal and corticobulbar tract)
- ipsilateral hemiparesis (herniation)
- contralateral hemiparesis (cerebral crus)

35
Q

Why may a herniating uncus result in a dilated pupil before it progresses to become in the down and out position with ptosis?

A

PS fibres surround motor fibres of CNIII therefore will be compressed first

36
Q

Tonsillar herniation (coning) is considered to be the most severe herniation. It compresses the medulla and therefore which regulatory centres?

A

Respiratory

Cardiac

37
Q

Projective vomiting can be a later stage of raised ICP, what causes this?

A

Good question sir - me don’t know. Something to do with the vomiting centres??

38
Q

What is decorticate posturing? What is it a sign of?

A

Damage of one/both corticospinal tracts

  • Arms are adducted, flexed with wrist/finger flexed on the chest
  • Legs are stiffly extended and internally rotated
  • plantar flexion
39
Q

What is decerebrate posturing? What is it a sign of?

A

Damage to upper brain stem

  • Arms: adducted, extended
  • Wrists: pronated, fingers flexed
  • Legs: stiffly extended, plantar flexion
40
Q

What is a subarachnoid haemorrhage?

A

Bleed within subarachnoid space (between arachnoid and pia mater)
Presentation: severe, sudden onset headache and vomiting.

41
Q

What is an extradural haemorrhage?

A

Bleeding into extradural space (between skull and endosteal layer of dura mater)
Often hit head on pterion (middle meningeal artery), lucid period then collapse (younger people - dura gets thicker as get older so extradural more common in younger people)

Biconvex shape, limited by cranial sutures but not by venous sinuses.

42
Q

What is a subdural haemorrhage?

A

Bleeding into subdural space (between meningeal layer of dura mater and arachnoid mater). Shearing of bridging veins that drain into adjacent dural sinus - elderly people, falls

43
Q

What is a brain contusion?

A

Foci of superficial bruising of the brain

44
Q

Where do brain contusions often occur?

A

On crests of gyri: brain moves over roughened floor of skull

  • inferior surface of frontal lobe
  • lateral/inferior surface of temporal lobe
  • region adjacent to lateral fissures
  • orbital poles
45
Q

Define ‘coup’ and ‘contra-coup’ injuries

A

Coup: point of impact

Contra-coup: traumatic axonal and neuronal damage distant to primary impact -> result of stresses on decelerating brain when it collides with inside of skull

46
Q

What is the difference between diffuse and focal brain injury?

A

Diffuse: microscopic damage, can’t be seen on imaging e.g.

  • diffuse axonal injury (DAI)
  • diffuse brain swelling
  • hypoxic-ischaemic damage
  • diffuse vascular injury

Focal: pathology seen on CT/MRI -> neurosurgically treatable

  • contusion/laceration to scalp
  • fracture to skull
  • haemorrhage/infection to meninges
  • infection/laceration/haemorrhage/contusion to brain
47
Q

What is ‘diffuse axonal injury’ and what are its causes?

A

Result of shearing forces, typically from rotational acceleration (often deceleration). Shearing due to change in velocity has a predilection for axons at the grey-white matter junction. The forces often result in damage to the cells and result in oedema. Complete tearing of the axons is only seen in severe cases.

Damage is more widespread than focal brain injury. Extensive lesions in white matter tracts -> LOC and vegetative state

Outcome is frequently coma: more than 90% with DAI never regain consciousness :(

DAI - most common and devastating head injury

48
Q

How is DAI classified?

A

Grade I: involves grey-white matter interfaces

Grade II: Involves corpus callosum and stage I

Grade III: involves brainstem + grade I and II locations

MRI is best imaging

Session 3: skull base & head (4 decks)

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