Neurotrauma Flashcards

1
Q

Breathing patterns associated with damage to

a) cerebrum
b) pons
c) medulla

A

a) Cheyne stokes (alternating hyperpneoa and apnoea)
b) apneustic (prolonged pause at end inspiration)
c) ataxic (irregular in rate and volume)

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2
Q

How is the size of an intracerebral haematoma calculated

A

(a x b x c) / 2
a=maximum haematoma diameter
b=haematoma diameter at 90 degrees to a
c=number of CT slides with haematoma visible x slice thickness

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3
Q

How is CPP calculated

A

MAP - ICP

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4
Q

How is MAP calculated

A

2/3 diastole + 1/3 systole

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5
Q

In which patients should ICP be monitored

A

GCS 3-8 with abnormal CT

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6
Q

How is RICP managed?

A
ventilate and oxygenate
keep CO2 at the low end of normal (4)
nurse at 30 degree angle
mannitol 100ml 20%
paralyse (to reduce cerebral O2 requirements)
normoglycaemia 
phenytoin for seizures
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7
Q

What are the advantages and disadvantages of paralysing a patient in RICP management?

A

reduces cerebral O2 requirements
allows TTM
can’t assess any progress

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8
Q

Define mild, moderate and severe TBI according to GCS

A

mild: 14-15
mod: 9-13
severe: <9

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9
Q

What is a primary head injury

A

Injury occurring at the time of the impact. Can be vascular, neuronal, axonal

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10
Q

What is a secondary head injury

A

processes occurring later down the line that has been triggered by the primary head injury

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11
Q

State some examples of processes that can occur as part of a secondary head injury

A
ischaemia
hypoxia
neuroinflammation (cytokines and chemokines)
RICP
infection
seizures
mitochondrial dysfunction
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12
Q

What is a tertiary/late secondary head injury

A

injury occurring years after the primary injury. Thought to be due to proteinopathies. Patients can present with MND, Parkinsons, alzheimers, fronto-temporal dementia

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13
Q

What are some faults with GCS

A

skewed important to motor
can’t assess if facial/ocular injury
can’t assess if intubated
designed for purely head injured patients

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14
Q

Talk through the eye component of GCS

A

4: spontaneous eye opening
3: open to verbal command
2: open to pain
1: no response

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15
Q

Talk through the verbal component of GCS

A

5: orientated
4: confused
3: inappropriate words
2: incomprehensible sounds
1: no response

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16
Q

Talk through the motor component of GCS

A

6: spontaneous movements
5: localise pain
4: withdraw from pain
3: flexion (decorticate)
2: extension (decerebrate)
1: no response

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17
Q

What should you examine in a possible head injury patient

A
breathing pattern
pupils 
ocular movements (cranial nerves)
c-spine 
auscultate the carotids
limb movements and power
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18
Q

Indications for a CT after a head injury

A
GCS <13
GCS <15 after 2 hours
>1 episode of vomiting
open, depressed or basal skull fracture
seizure
focal deficit
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19
Q

Compare the appearance of a T1 and T2 weighted MRI

A

T1: black CSF. Grey matter is grey and white matter is white
T2: bright CSF. Grey matter is white and white matter is grey

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20
Q

What does acute and hyperacute blood look like on a CT

A

acute is hyperdense (bright)

hyperacute can appear as a darker patch within the bright acute bleed

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21
Q

What motion often causes DAI

A

rotational

acceleration/deceleration

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22
Q

What is the pathophysiology of DAI

A

sheering of G/W matter interface

wallerian degeneration distal to the sheering forces

23
Q

What is the CT appearance of DAI

A

homogenous loss of G/W matter interface

scattered punctae

24
Q

What is a cerebral contussion

A

microhaemorrhages and small vessel leaks

They are <1cm

25
Q

where are contussions most likely to occur

A

inferior frontal
temporal poles
these are both sharp and ridgy areas

26
Q

State some clinical features suggestive of a basal skull fracture

A
racoon eyes
battles sign
CSF rhinorrhoea and ottorhoea
haemotympanum 
CN signs
27
Q

Where is a basal skull fracture most likely to occur

A

longitudinal fracture of the petrous part of the temporal bone

28
Q

what is a concussion

A

temporary alteration of consciousness
no structural damage
absence of a penetrating injury

29
Q

compare the bleeding source associated with extradural vs subdural vs subarachnoid haematomas

A

extra: middle meningeal artery or DVS
subdural: cortical bridging veins
subarachnoid: berry anneurysm, AV malformation

30
Q

what is the likely source of bleeding in a posterior fossa bleed

A

DVS

31
Q

where does the middle meningeal artery originate and which foramen does it travel through

A
maxillary artery (branch of ECA)
foramen spinosum
32
Q

describe the clinical presentation of extradural, subdural and subarachnoid haemorrhages

A

extra: lucid interval
subdural: presents like an evolving stroke
subarachnoid: occipital thunderclap headache

33
Q

Describe the CT of an extradural haematoma

A

lenticuloform

limited by suture lines

34
Q

describe the CT of a subdural haematoma

A

crescent
not limited by suture lines
can enter sulci
loss of G/W matter interface

35
Q

describe the CT of a subarachnoid haematoma

A

hyperdense basal cisterns and sulci

36
Q

What 2 mechanisms lead to ischaemia in secondary brain injury

A

blood is an irritant so get vasospasm

RICP leads to reduced CPP

37
Q

how does cerebral oedema occur in secondary brain injury

A

extracellular to intracellular because of NaK pump failure

intravascular to interstitial because of BBB breakdown

38
Q

Describe the Monro-Kellie hypothesis

A

Pressure-volume relationship aiming to keep a dynamic equilibrium among non-compressible components in a rigid skull.
Components within the fixed rigid skull will compensate for an increased intracranial volume up until a point at which ICP begins to rise

39
Q

What are the x and y axis on the monro-kellie graph

A

x: intracranial volume
y: ICP

40
Q

Describe cushings reflex

A

Hypertension: brainstem compression stimulates sympathetics to try and overcome the ICP and maintain CPP
Bradycardia: in response to the hypertension the carotid sinus stimulates a vagal response
reduced RR: ischaemia of the respiratory centers in the brainstem

41
Q

State the types of herniation syndrome

A

subfalcine
uncul
tonsillar

42
Q

what is compressed in a subfalcine herniation and what does this result in clinically

A

the cingulate gyrus is compressed under the falx cerebri

ACA compressed leading to contralateral leg weakness

43
Q

what is compressed in a uncal herniation and what does this result in clinically

A

uncus of the temporal lobe
CN3: ipsilateral dilated, down and out pupil
CN6: diplopia
reticular formation: reduced GCS
cerebellar peduncle: contralateral hemiparesis

44
Q

Describe kernohans phenomenon

A

contra-lateral cerebellar peduncle compressed where the descending motor tracts are located giving ipsilateral (to the lesion) motor weakness

45
Q

what is compressed in a tonsillar herniation and what does this result in clinically

A

cerebellar tonsils compressed through the foramen magnum

cardioresp centres in medulla compressed

46
Q

How can ICP be measured

A

ICP bolt
intraventricular catheter
intraparenchymal pressure monitor

47
Q

Define secondary brain injury

A

progressive series of complex, interconnected, biochemical events all ending in neuronal death

48
Q

craniotomy vs craniectomy

A

craniotomy: bone is replaced
craniectomy: bone is left off and the skin flap closed

49
Q

what are mayfield pins

A

hold the head in place whilst a craniectomy/otomy is performed

50
Q

why do burr holes tend not to work in haematoma management

A

because the blood is thick and clotted

51
Q

which type of haematoma might a burr hole work and why

A

chronic subdural when the blood has gone back to a liquid

52
Q

what is secondary impact syndrome

A

seen in younger patients

following a concussion there is malignant oedema

53
Q

anterograde vs retrograde amnesia

A

anterograde: can’t form new memories
retrograde: inability to recall past memories

54
Q

when should a neurosurgeon become involved in head injury patients

A
GCS <8 or deteriorating
Confusion >4 hours
progressive focal neurological signs
seizure without full recovery
depresed skull fracture
penetrating injury
CSF leakage