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4th year passmedicine by topic > Neurosurgery > Flashcards

Neurosurgery Flashcards

1
Q

Criteria for brain stem death testing

A

Deep coma of known aetiology
Reversible causes excluded
No sedation
Normal electrolytes

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2
Q

Testing for brain death should be undertaken by whom?

A

two appropriately experienced doctors on two separate occasions

other should be experienced in performing brain stem death testing and have at least 5 years post-graduate experience. One of them must be a consultant.

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3
Q

members of transplant team cannot confirm brain stem death

A

true

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4
Q

Testing for brain death - eyes

A

Fixed pupils which do not respond to sharp changes in the intensity of incident light

No corneal reflex

Absent oculo-vestibular reflexes

No response to supraorbital pressure

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5
Q

Testing for brain death - breathing/pharynx

A

No cough reflex to bronchial stimulation or gagging response to pharyngeal stimulation

No observed respiratory effort in response to disconnection of the ventilator

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6
Q

oculo-vestibular reflexes are tested how?

A

slow injection of at least 50ml of ice-cold water into each ear in turn (the caloric test)

  • no eye movements = absent reflexes
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7
Q

Describe the following type of herniation: Subfalcine

A

Displacement of the cingulate gyrus under the falx cerebri

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8
Q

Describe the following type of herniation: Central

A

Downwards displacement of the brain

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9
Q

Describe the following type of herniation: Transtentorial / uncal herniation

A

Displacement of the uncus of the temporal lobe under the tentorium cerebelli.

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10
Q

Describe the clinical consequences of uncal/transtentorial herniation

A

parasympathetic compression of the third cranial nerve - ipsilateral dilated pupil

ompression of the cerebral peduncle - contralateral paralysis

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11
Q

Describe the following type of herniation: Tonsillar

A

Displacement of the cerebellar tonsils through the foramen magnum

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12
Q

Tonsillar herniation is also called coning

A

true

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13
Q

tonsillar herniation/coning in raised ICP results in?

A

compression of the cardiorespiratory centre

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14
Q

tonsillar herniation/coning in chiari 1 malformation is seen without raised ICP

A

true

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15
Q

Describe the following type of herniation: Transcalvarial

A

Occurs when brain is displaced through a defect in the skull (e.g. a fracture or craniotomy site)

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16
Q

The brain autoregulates its blood supply

A

true

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17
Q

as ICP rises you get increasingly hypotensive systemically

A

false

systemic circulation will display changes to try and meet the perfusion needs of the brain. Usually this will involve hypertension.

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18
Q

if ICP compresses the brain what are the consequences?

A

cranial nerve palsies

compression of essential centres in the brain stem will occur. When the cardiac centre is involved bradycardia will often develop.

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19
Q

Extradural haematoma Often results from

A

acceleration-deceleration trauma or a blow to the side of the head

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20
Q

The majority of extradural haematomas occur where?

A

The majority of extradural haematomas occur in the temporal region where skull fractures cause a rupture of the middle meningeal artery.

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21
Q

Extradural haematoma may have a lucid interval

A

true

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22
Q

Subdural haematoma Most commonly occur around the

A

frontal and parietal lobes

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23
Q

subdural has a slower/faster onset of symptoms compared to extrafural haematoma

A

slower

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24
Q

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.

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25
Q

Pathophysiology of haematoma?

A

Primary brain injury may be focal (contusion/ haematoma) or diffuse (diffuse axonal injury)
Diffuse axonal injury occurs as a result of mechanical shearing following deceleration, causing disruption and tearing of axons
Intra-cranial haematomas can be extradural, subdural or intracerebral, while contusions may occur adjacent to (coup) or contralateral (contre-coup) to the side of impact
Secondary brain injury occurs when cerebral oedema, ischaemia, infection, tonsillar or tentorial herniation exacerbates the original injury. The normal cerebral auto regulatory processes are disrupted following trauma rendering the brain more susceptible to blood flow changes and hypoxia
The Cushings reflex (hypertension and bradycardia) often occurs late and is usually a pre terminal event

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26
Q

Where there is life threatening rising ICP such as in extradural haematoma and whilst theatre is prepared or transfer arranged use of IV ? may be required.

A

mannitol/ frusemide

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27
Q

Diffuse cerebral oedema may require

A

decompressive craniotomy

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28
Q

in head injury Hyponatraemia is most likely to be due to the syndrome of inappropriate ADH secretion.

A

true

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29
Q

Minimum cerebral perfusion pressure in adults and children?

A

Minimum of cerebral perfusion pressure of 70mmHg in adults.

Minimum cerebral perfusion pressure of between 40 and 70 mmHg in children.

30
Q

ICP monitoring is indicated when?

A

ICP monitoring is appropriate in those who have GCS 3-8 and normal CT scan.
ICP monitoring is mandatory in those who have GCS 3-8 and abnormal CT scan.

31
Q

Interpretation of pupillary findings in head injuries:

Unilaterally dilated Light response - Sluggish or fixed

A

3rd nerve compression secondary to tentorial herniation

32
Q

Interpretation of pupillary findings in head injuries:

Bilaterally dilated Light response - Sluggish or fixed

A

Poor CNS perfusion

Bilateral 3rd nerve palsy

33
Q

Interpretation of pupillary findings in head injuries:
Unilaterally dilated or equal
Light response: Cross reactive (Marcus - Gunn)

A

Optic nerve injury

34
Q

Interpretation of pupillary findings in head injuries:

Bilaterally constricted

A

Opiates
Pontine lesions
Metabolic encephalopathy

35
Q

Interpretation of pupillary findings in head injuries:
Unilaterally constricted
Light response preserved

A

Sympathetic pathway disruption

36
Q

Head injury - NICE guidance on investigation:

CT head immediately
which GCS scores?

A

GCS < 13 on initial assessment

GCS < 15 at 2 hours post-injury

37
Q

Head injury - NICE guidance on investigation:

CT head immediately
which fractures?

A

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).

38
Q

Head injury - NICE guidance on investigation:

CT head immediately
how many episodes of vomitings?

A

MORE than 1 episode of vomiting

39
Q

Head injury - NICE guidance on investigation:

CT head immediately if they have a seizure

A

true

40
Q

Head injury - NICE guidance on investigation:

CT head immediately if they have focal eurological deficit

A

true

41
Q

CT head scan within 8 hours of the head injury - for adults with any of the following risk factors who have experienced some loss of consciousness or amnesia since the injury:

A

age 65 years or older
any history of bleeding or clotting disorders
dangerous mechanism of injur
more than 30 minutes’ retrograde amnesia of events immediately before the head injury

42
Q

If a patient is on warfarin who have sustained a head injury with no other indications for a CT head scan, perform a CT head scan within ?hours of the injury.

A

8 hours

43
Q

Intracerebral haematoma CT imaging will show

A

hyperdensity (bright lesion) within the substance of the brain.

44
Q

Hydrocephalus is defined as

A

excessive volume of cerebrospinal (CSF) fluid within the ventricular system of the brain and is caused by an imbalance between CSF production and absorption.

45
Q

Patients with hydrocephalus present with symptoms due to raised intracranial pressure, which include:

A

Headache (typically worse in the morning, when lying down and during valsalva)
Nausea and vomiting
Papilloedema
Coma (in severe cases)

46
Q

Children with severe hydrocephalus also classically present with

A

failure of upward gaze (‘sunsetting’ eyes)

47
Q

Hydrocephalus can be broadly divided into two categories

A

Obstructive (‘non-communicating’) hydrocephalus

Non-obstructive (‘communicating’) hydrocephalus

48
Q

Obstructive hydrocephalus is

A

due to a structural pathology blocking the flow of cerebrospinal fluid. Dilatation of the ventricular system is seen superior to site of obstruction.

49
Q

Obstructive hydrocephalus causes?

A

tumours, acute haemorrhage (e.g. subarachnoid haemorrhage or intraventricular haemorrhage) and developmental abnormalities (e.g. aqueduct stenosis).

50
Q

Non-obstructive hydrocephalus is

A

due to an imbalance of CSF production absorption. It is either caused by an increased production of CSF (e.g. choroid plexus tumour (very rare)) or more commonly a failure of reabsorption at the arachnoid granulations (e.g. meningitis or post-haemorrhagic).

51
Q

Normal pressure hydrocephalus is

A

unique form of non-obstructive hydrocephalus characterised by large ventricles but normal intracranial pressure. The classic triad of symptoms is dementia, incontinence and disturbed gait.

52
Q

Hydrocephalus first line ix?

A

CT head

MRI may be used to investigate hydrocephalus in more detail

53
Q

Hydrocephalus what is both diagnostic and therapeutic

A

Lumbar puncture

54
Q

Treatment hydrocephalus

A

external ventricular drain (EVD) is used in acute, severe hydrocephalus

ventriculoperitoneal shunt (VPS) is a long-term CSF diversion technique

55
Q

most common cause of SAH is head injury and this is called traumatic SAH . In the absence of trauma, SAH is termed

A

spontaneous SAH

56
Q

Causes of spontaneous SAH include:

A 
Intracranial aneurysm 85%
Arteriovenous malformation
Pituitary apoplexy
Arterial dissection
Mycotic (infective) aneurysms
Perimesencephalic (an idiopathic venous bleed)
57
Q

Conditions associated with berry aneurysms include

A

adult polycystic kidney disease, Ehlers-Danlos syndrome and coarctation of the aorta

58
Q

Classical presenting features include: SAH

A

Headache: typically sudden-onset (‘thunderclap’ or ‘baseball bat’), severe (‘worst of my life’) and occipital
Nausea and vomiting
Meningism (photophobia, neck stiffness)
Coma
Seizures
Sudden death
ECG changes including ST elevation may be seen

59
Q

Computed tomography (CT) head shows what in SAH

A 
Acute blood (hyperdense/bright on CT)
CT is negative for SAH (no blood seen) in 7% of cases.
60
Q

What is Used to confirm SAH if CT is negative?

A

Lumbar puncture

61
Q

CSF findings consistent with subarachnoid haemorrhage include ?

A

normal or raised opening pressure

xanthochromia

62
Q

LP should be performed when in SAH?

A

LP is performed at least 12 hours following the onset of symptoms to allow the development of xanthochromia (the result of red blood cell breakdown).

63
Q

Referral to neurosurgery to be made as soon as SAH is confirmed

A

TRUE

64
Q

After spontaneous SAH is confirmed, the aim of investigation is to identify a causative pathology that needs urgent treatment:
FURTHER IX?

A

CT intracranial angiogram (to identify a vascular lesion e.g. aneurysm or AVM)
+/- digital subtraction angiogram (catheter angiogram)

65
Q

Most intracranial aneurysms are now treated with a

A

coil

66
Q

Until the aneurysm is treated, the patient should be kept on strict bed rest, well-controlled blood pressure and should avoid straining in order to prevent a re-bleed of the aneurysm

A

true

67
Q

anuerysmal SAH - Vasospasm is prevented using

A

21-day course of nimodipine

68
Q

aneurysmal SAH vasospasm mx

A

hypervolaemia, induced-hypertension and haemodilution

69
Q

Complications of aneurysmal SAH:

A

Re-bleeding
happens in around 10% of cases and most common in the first 12 hours

Vasospasm (also termed delayed cerebral ischaemia), typically 7-14 days after onset

Hyponatraemia (most typically due to syndrome inappropriate anti-diuretic hormone (SIADH))
Seizures
Hydrocephalus
Death

70
Q

Important predictive factors in SAH:

A

conscious level on admission
age
amount of blood visible on CT head

4th year passmedicine by topic (96 decks)

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